No abstract

Objective: Characterize relationships among substance misuse, depression, employment, and suicidal ideation (SI) following moderate to severe traumatic brain injury (TBI). Design: Prospective cohort study. Setting: Inpatient rehabilitation centers with telephone follow-up; level I/II trauma centers in the United States. Participants: Individuals with moderate to severe TBI with data in both the National Trauma Data Bank and the Traumatic Brain Injury Model Systems National Database, aged 18 to 59 years, with SI data at year 1 or year 2 postinjury (N = 1377). Main Outcome Measure: Primary outcome of SI, with secondary employment, substance misuse, and depression outcomes at years 1 and 2 postinjury. Results: Cross-lagged structural equation modeling analysis showed that year 1 unemployment and substance misuse were associated with a higher prevalence of year 1 depression. Depression was associated with concurrent SI at years 1 and 2. Older adults and women had a greater likelihood of year 1 depression. More severe overall injury (injury severity score) was associated with a greater likelihood of year 1 SI, and year 1 SI was associated with a greater likelihood of year 2 SI. Conclusions: Substance misuse, unemployment, depression, and greater extracranial injury burden independently contributed to year 1 SI; in turn, year 1 SI and year 2 depression contributed to year 2 SI. Older age and female sex were associated with year 1 depression. Understanding and mitigating these risk factors are crucial for effectively managing post-TBI SI to prevent postinjury suicide.

No abstract

Background Cognitive dysfunction adversely effects multiple functional outcomes and social roles after TBI. We hypothesize that chronic systemic inflammation exacerbates cognitive deficits post-injury and diminishes functional cognition and quality of life (QOL). Yet few studies have examined relationships between inflammation and cognition after TBI. Associations between early chronic serum inflammatory biomarker levels, cognitive outcomes, and QOL 6-months and 12-months after moderate-to-severe TBI were identified using unweighted (uILS) and weighted (wILS) inflammatory load score (ILS) formation. Methods Adults with moderate-to-severe TBI (n ​= ​157) completed neuropsychological testing, the Functional Impairment Measure Cognitive Subscale (FIM-Cog) and self-reported Percent Back to Normal scale 6 months (n ​= ​139) and 12 months (n ​= ​136) post-injury. Serial serum samples were collected 1–3 months post-TBI. Cognitive composite scores were created as equally weighted means of T-scores derived from a multidimensional neuropsychological test battery. Median inflammatory marker levels associated with 6-month and 12-month cognitive composite T-scores (p ​< ​0.10) were selected for ILS formation. Markers were quartiled, and quartile ranks were summed to generate an uILS. Marker-specific β-weights were derived using penalized ridge regression, multiplied by standardized marker levels, and summed to generate a wILS. ILS associations with cognitive composite scores were assessed using multivariable linear regression. Structural equation models assessed ILS influences on functional cognition and QOL using 12-month FIM-Cog and Percent Back to Normal scales. Results ILS component markers included: IL-1β, TNF-α, sIL-4R, sIL-6R, RANTES, and MIP-1β. Increased sIL-4R levels were positively associated with overall cognitive composite T-scores in bivariate analyses, while remaining ILS markers were negatively associated with cognition. Multivariable receiver operator curves (ROC) showed uILS added 14.98% and 31.93% relative improvement in variance captured compared to the covariates only base model (age, sex, education, Glasgow Coma Scale score) when predicting cognitive composite scores at 6 and 12 months, respectively; wILS added 33.99% and 36.87% relative improvement in variance captured. Cognitive composite mediated wILS associations with FIM-Cog scores at 12 months, and both cognitive composite and FIM-Cog scores mediated wILS associations with QOL. Conclusions Early chronic inflammatory burden is associated with cognitive performance post-TBI. wILS explains greater variance in cognitive composite T-scores than uILS. Linking inflammatory burden associated with cognitive deficits to functional outcome post-TBI demonstrates the potential impact of immunotherapy interventions aimed at improving cognitive recovery post-TBI.

No abstract