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

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 C^15O 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.