Table 1.

Published studies in experimental and human stroke studies evaluating ¹⁸F-FDG uptake.

Study	Stroke model/number of patients	Procedures	Poststroke timing	Relevant findings
Animals
Walberer et al., 2012 [54]	Embolic MCAO in rats	18F-FDG PET     MRI and histological examination (final infarct volume)     15O-H2O PET (CBF)	75 minutes 24 hours Before, and at 5, 30, and 60 minutes	(i) At 60 minutes, rCBF correlated positively with K1 (FDG transport from blood to brain). (ii) Infarcted tissue at 24 hours could be predicted by Ki (net influx rate constant) at 75 min. (iii) Parts of hypoperfused tissue that was infarcted at 24 hours had normal or elevated Ki at 1 hour.
Sobrado et al., 2011 [55]	Transient and permanent MCAO in rats	18F-FDG PET     MRI (T2WI, DWI and PWI) Nissl staining	Before and at 3, 24, and 48 hours 3 hours	(i) 18F-FDG uptake in ischemic core regions was reduced for all time points after MCAO. (ii) At 3 hours after MCAO, areas that recovered with reperfusion at 24 hours had greater 18F-FDG uptake when compared to brain areas that progressed to infarction at 24 hours.
Kuge et al., 2000 [57]	Thromboembolic MCAO in primates	18F-FDG PET   12O-H2O PET (CBF) 2,3,5-triphenyltetrazolium chloride (TTC) staining	24 hours Before and 1, 2, 4, 6, and 24 hours 24 hours	(i) Ischemic core: reduced CBF, CMRglc, and negative TCC. (ii) Ischemic penumbra: moderate decrease of CBF, increase of CMRglc, and positive TCC staining.
Fukumoto et al., 2011 [58]	Thrombotic MCAO in rats	18F-FDG PET   11C-PK11195 PET (neuroinflammation)    11C-FMZ PET (neuronal integrity)    11C-PK11195; 11C-FMZ and 18F-FDG autoradiography   Iba1 (microglia activation) and NeuN (neuronal damage) immunohistochemistry	Before and days 1, 3, 7, and 14   7 days	(i) Peri-infarct areas: significantly increased PET uptake of 18F-FDG at days 7 and 14 and of 11C-PK11195 at days 3, 7, and 14, plus Iba1 staining at day 7. (ii) Infarct core: reduced uptake of 18F-FDG at days 1–14, increased 11C-(R)PK11195 bindings at days 7 and 14 and reduced 11C-FMZ binding at days 7 and 14.
Humans
Heiss et al., 1992 [40]	16 hemispheric stroke patients	18F-FDG, H2 15O, 15O2, and C15O PET	6–48 hours   13–25 days	(i) Core: severely reduced OEF, CMRO2, CBF, and CMRglc. (ii) Penumbra: reduced CMRO2, CMRglc, and CBF. (iii) Some penumbral areas had increased CMRO2, OEF, CMRglc and GEF and did not progress to final infarct.    (iv) When compared to the first scan: Core—increased CBF; penumbra: reduced CMRO2, CMRglc, and OEF.
Nasu et al., 2002 [60]	24 ischemic stroke patients	18F-FDG PET, MRI, and CT	1–7 days Later time points	(i) In the acute phase 18F-FDG hyperaccumulation foci around hypoaccumulation areas were evident in 7 out of 20 patients. (ii) Final tissue fate of hyper-accumulation areas was variable.