Detection of brain amyloid β deposition in patients with neuropsychological impairment after traumatic brain injury: PET evaluation using Pittsburgh Compound-B

Objective: Traumatic brain injury (TBI) is an epigenetic risk factor for Alzheimer's disease (AD) and amyloid beta (A beta) deposition is observed histopathologically in the traumatized brain. This study was conducted to detect cerebral Ab deposition using amyloid positron emission tomography (PET) in patients with neuropsychological impairment after TBI. Methods: Twelve patients with post-traumatic neuropsychological impairment (11 men and one woman, age range = 21-78 years) were examined using Pittsburgh Compound B (C-11-PIB) PET at the chronic stage after TBI (range 5-129 months). Results: C-11-PIB was positive in three patients and negative in the other nine patients. There was no correlation between C-11-PIB deposition and the severity of injury; initial CT findings; elapsed time from the injury; and neuropsychological test scores. Conclusions: The absence of A beta deposition in many patients with chronic neuropsychological impairment after TBI does not support the premise that A beta pathology progresses over time in the traumatized brain. Early and sequential C-11-PIB PET examination may clarify the time course of A beta deposition in the traumatized brain and the relationship between traumatic brain insult and subsequent neuropsychological impairment.