Traumatic Encephalopathy Syndrome in the Late Effects of Traumatic Brain Injury (LETBI) Study Cohort.

Background and Objective: Traumatic encephalopathy syndrome (TES) is the proposed clinical manifestation of chronic traumatic encephalopathy (CTE) neuropathologic change secondary to repetitive head impacts (RHI). The prevalence of TES and its component symptoms is not known in individuals with single TBI, a subset of whom also have RHI. We used prospectively collected data to operationalize TES criteria and test the hypothesis that the core clinical features of TES are common among those with TBI, regardless of RHI exposure status and other demographic and injury characteristics. Methods: Secondary analysis of data from the Late Effects of TBI (LETBI) study, a community-based study of individuals with complicated mild, moderate, or severe TBI. Participants were categorized by TBI severity and presence of RHI, creating 6 groups (those with isolated mild, moderate, and severe TBI, with and without RHI). Chi-squared tests were used to compare the proportion of each group that met each of the core clinical criteria overall TES diagnosis. Binary logistic regression models were used to examine associations of demographic and injury characteristics on TES diagnosis. Results: In 295 participants with TBI, mean (SD) age 52.6(15.6) years and 35.6% female, 138 (46.8%) had RHI exposure meeting the TES criteria exposure threshold. In the full sample, 56.9%, 32.9% and 45.8% of participants met TES core criterion of cognitive impairment, neurobehavioral dysregulation, and progressive course of clinical features, respectively. Overall, 14.9% of the LETBI sample had substantial RHI exposure and met all 3 clinical features, meeting consensus-based TES criteria. When RHI exposure criterion was lifted, 33.5% of the LETBI sample with isolated TBI met all core clinical criteria. No injury or demographic variables predicted the likelihood of meeting TES Core Criteria (OR=3.02, p=0.10). Discussion: Rates of TES clinical features are high among TBI survivors with and without RHI, across injury severity groups. Presence of TES core clinical features was greatest among those with no RHI, suggesting that chronic and sometimes progressive clinical sequelae of TBI resemble TES, but may reflect a distinct pathobiological process. Limitations include possible selection of participants with chronic symptoms. Findings emphasize the centrality of RHI exposure to TES diagnostic criteria.