Interrogating changes in cerebral glucose availability, delivery, uptake and phosphorylation after traumatic brain injury; an (15)oxygen and F-18-fluorodeoxyglucose positron emission tomography study

Objectives Metabolic derangements are common after traumatic brain injury (TBI), but few studies have used multi-tracer positron emission tomography (PET) to interrogate underlying pathophysiology (1,2). We examined relationships between oxygen and glucose metabolism using 15oxygen (15O) and 18F-fluorodeoxyglucose (FDG) PET. Methods Twenty-six TBI patients underwent combined 15O and FDG-PET on 34 occasions; 10 and 18 healthy volunteers (controls) underwent 15O and FDG-PET respectively. FDG rate constants were determined with an irreversible two-compartment model: transport across BBB (K1,k2), hexokinase activity (k3), and influx rate (Ki). Regions of interest were defined for haemorrhagic lesion (core), hypodense tissue (penumbra), 1 cm border zone of normal appearing tissue (peri-penumbra), and remote normal appearing tissue (normal). Plasma and microdialysis glucose were recorded. Results In patients, glucose delivery (K1) was dependent on supply with significantly lower values occurring below a threshold cerebral blood flow (CBF) of 25ml/100ml/min. K1 was particularly driven by CBF within lesion core (R=0.87,p