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

Abstract

Objective: Traumatic brain injury (TBI) is an epigenetic risk factor for Alzheimer’s disease (AD) and amyloid β (Aβ) deposition is observed histopathologically in the traumatized brain. This study was conducted to detect cerebral Aβ 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 (¹¹C-PIB) PET at the chronic stage after TBI (range = 5–129 months).

Results: ¹¹C-PIB was positive in three patients and negative in the other nine patients. There was no correlation between ¹¹C-PIB deposition and the severity of injury; initial CT findings; elapsed time from the injury; and neuropsychological test scores.

Conclusions: The absence of Aβ deposition in many patients with chronic neuropsychological impairment after TBI does not support the premise that Aβ pathology progresses over time in the traumatized brain. Early and sequential ¹¹C-PIB PET examination may clarify the time course of Aβ deposition in the traumatized brain and the relationship between traumatic brain insult and subsequent neuropsychological impairment.

• Amyloid beta (β)
• neuropsychological impairment
• Pittsburgh Compound B
• positron emission tomography
• traumatic brain injury

Acknowledgements

We are grateful for the excellent technical support of the radiological technologist at our institution.