Delayed-onset after-effects, which manifest years after an injury, is a current topic of discussion in the field of traumatic brain injury. Some traumatic brain injury cases involve a cognitive function decline starting anywhere from several years to decades post brain injury. Unfortunately, there is currently little understanding of how traumatic brain injury brings about delayed-onset neuropsychiatric symptoms. In recent years, positron emission tomography has improved our ability to detect amyloid and tau lesions. These advances are expected to enable the detection of traumatic brain injury-caused delayed-onset pathologies in alive patients as well as the evaluation of the pathological mechanisms underlying these conditions. The elucidation of the pathophysiology of late-onset cognitive psychiatric symptoms will greatly benefit the diagnosis and treatment of patients with traumatic brain injury. Here, we will focus on an emblematic delayed-onset pathology often seen after traumatic brain injury—Alzheimer’s disease—and explain its relationship with chronic traumatic encephalopathy.
Diagnosis and Treatment of Traumatic Brain Injury, 2022, Pages 27-38