Abstract
Traumatic brain injury (TBI) is common, and is often the leading cause of disability and death. Complications after TBI include increased risk for chronic central nervous system disease, such as Alzheimer's disease (AD). However, the pathophysiology relating acute injury to neurodegeneration is unclear. Here we present a case of a patient whose cognition declined after TBI, and whose 18F fluorodeoxyglucose positron emission tomography scan showed an AD pattern.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
