Widespread and prolonged increase in (R)-(11)C-PK11195 binding after traumatic brain injury

Our objective was to measure (R)-(11)C-PK11195 binding as an indirect marker of neuronal damage after traumatic brain injury (TBI). Dynamic (R)-(11)C-PK11195 PET scans were acquired for 8 patients 6 mo after TBI and for 7 age-matched healthy controls. (R)-(11)C-PK11195 binding was assessed using the simplified reference tissue model. Because of widespread traumatic changes in TBI, an anatomic reference region could not be defined. Therefore, supervised cluster analysis was used to generate an appropriate reference tissue input. Increased whole-brain binding of (R)-(11)C-PK11195 was observed in TBI patients. Regional analysis indicated that increased (R)-(11)C-PK11195 binding was widespread over the brain. Six months after TBI, there was a prolonged and widespread increase in (R)-(11)C-PK11195 binding, which is indicative of diffuse neuronal damage