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Acute Changes in Regional Cerebral ¹⁸F-FDG Kinetics in Patients with Traumatic Brain Injury

¹ Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California
² Brain Injury Research Center, Division of Neurosurgery, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California

During the acute phase after traumatic brain injury (TBI), the metabolic state is regionally heterogeneous. The purpose of this study was to characterize contusional, pericontusional, and remote regions of TBI by estimating glucose transporter and hexokinase activities on the basis of ¹⁸F-FDG kinetic modeling. Methods: A standard 2-compartment model was used to measure ¹⁸F-FDG kinetic parameters in 21 TBI patients with cerebral contusions studied during the acute phase (3.1 ± 2.1 [mean ± SD] d after injury). Nineteen patients also underwent ¹⁵O-water PET to measure regional cerebral blood flow (CBF). A control study (¹⁸F-FDG and ¹⁵O-water) was done with 18 healthy volunteers. The rate constants K_i, K₁, and k₃ were assumed to represent the uptake, transport, and hexokinase activity of ¹⁸F-FDG, respectively; K_i was calculated as K₁ x [k₃/(k₂ + k₃)]. Results: The areas of contusional and pericontusional tissues located 4.5, 13.5, and 22.5 mm away from the contusion (PC_4.5, PC_13.5, and PC_22.5, respectively) demonstrated significantly reduced K₁ values, whereas the K₁ values for remote areas remained normal. The k₃ values were significantly reduced regardless of the distance from the contusion. Pericontusional areas with CT- or MRI-evidenced tissue damage showed significantly lower K_i (P < 0.001), CBF (P < 0.01), and K₁ (P < 0.0001) values than did areas without such damage, whereas the k₃ values did not differ significantly. Seven patients showed regionally increased ¹⁸F-FDG uptake (hot spots) in pericontusional areas. The k₃ value for the hot spots (0.086 ± 0.024/min) was significantly higher than that for the remote cortex (P < 0.01), whereas the K_i, CBF, and K₁ values did not show significant differences. Patients with hot spots showed significantly higher K_i and k₃ values in PC_4.5 (P < 0.05) and higher k₃ values in PC_22.5 (P < 0.05) than did patients without hot spots, whereas the K₁ and CBF values did not differ significantly. Conclusion: Brain tissue ¹⁸F-FDG kinetics in TBI patients were consistent with reduced hexokinase activity in the whole brain (including apparently uninjured cortex), whereas glucose transport was impaired only in the area immediately around the contusion. Pericontusional high levels of ¹⁸F-FDG uptake observed in a subgroup of patients could have been the result of regionally increased hexokinase activity.

Key Words: neurology • PET • traumatic brain injury • glucose transporter • hexokinase;¹⁸F-FDG

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