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.
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