Michael L Alosco1, Yorghos Tripodis2, Zachary H Baucom2, Jesse Mez2, Thor D Stein2, Brett Martin2, Olivia Haller2, Shannon Conneely2, Michael McClean2, Rachel Nosheny2, Scott Mackin2, Ann C McKee2, Michael W Weiner2, Robert A Stern2. 1. From the Departments of Neurology (M.L.A., J.M., O.H., S.C., A.C.M., R.A.S.), Pathology & Laboratory Medicine (T.D.S., A.C.M.), Boston University Alzheimer's Disease Center and CTE Center (Y.T., B.M.), and Departments of Neurosurgery (R.A.S.) and Anatomy and Neurobiology (R.A.S.), Boston University School of Medicine; Department of Biostatistics (Y.T., Z.H.B.), Biostatistics and Epidemiology Data Analytics Center (B.M.), and Department of Environmental Health (M.M.), Boston University School of Public Health, MA; VA Boston Healthcare System (T.D.S., A.C.M.); Department of Veterans Affairs Medical Center (T.D.S., A.C.M.), Bedford, MA; Departments of Psychiatry (R.N., S.M., M.W.W.), Radiology (M.W.W.), Biomedical Imaging (M.W.W.), Medicine (M.W.W.), and Neurology (M.W.W.), University of California, San Francisco; and Department of Veterans Affairs Medical Center (R.N., S.M., M.W.W.), Center for Imaging and Neurodegenerative Diseases, San Francisco, CA. malosco@bu.edu. 2. From the Departments of Neurology (M.L.A., J.M., O.H., S.C., A.C.M., R.A.S.), Pathology & Laboratory Medicine (T.D.S., A.C.M.), Boston University Alzheimer's Disease Center and CTE Center (Y.T., B.M.), and Departments of Neurosurgery (R.A.S.) and Anatomy and Neurobiology (R.A.S.), Boston University School of Medicine; Department of Biostatistics (Y.T., Z.H.B.), Biostatistics and Epidemiology Data Analytics Center (B.M.), and Department of Environmental Health (M.M.), Boston University School of Public Health, MA; VA Boston Healthcare System (T.D.S., A.C.M.); Department of Veterans Affairs Medical Center (T.D.S., A.C.M.), Bedford, MA; Departments of Psychiatry (R.N., S.M., M.W.W.), Radiology (M.W.W.), Biomedical Imaging (M.W.W.), Medicine (M.W.W.), and Neurology (M.W.W.), University of California, San Francisco; and Department of Veterans Affairs Medical Center (R.N., S.M., M.W.W.), Center for Imaging and Neurodegenerative Diseases, San Francisco, CA.
Abstract
OBJECTIVE: To test the hypothesis that repetitive head impacts (RHIs), like those from contact sport play and traumatic brain injury (TBI) have long-term neuropsychiatric and cognitive consequences, we compared middle-age and older adult participants who reported a history of RHI and/or TBI with those without this history on measures of depression and cognition. METHODS: This cross-sectional study included 13,323 individuals (mean age, 61.95; 72.5% female) from the Brain Health Registry who completed online assessments, including the Ohio State University TBI Identification Method, the Geriatric Depression Scale (GDS-15), and the CogState Brief Battery and Lumos Labs NeuroCognitive Performance Tests. Inverse propensity-weighted linear regressions accounting for age, sex, race/ethnicity, and education tested the effects of RHI and TBI compared to a non-RHI/TBI group. RESULTS: A total of 725 participants reported RHI exposure (mostly contact sport play and abuse) and 7,277 reported TBI (n = 2,604 with loss of consciousness [LOC]). RHI (β, 1.24; 95% CI, 0.36-2.12), TBI without LOC (β, 0.43; 95% CI, 0.31-0.54), and TBI with LOC (β, 0.75; 95% CI, 0.59-0.91) corresponded to higher GDS-15 scores. While TBI with LOC had the most neuropsychological associations, TBI without LOC had a negative effect on CogState Identification (β, 0.004; 95% CI, 0.001-0.01) and CogState One Back Test (β, 0.004; 95% CI, 0.0002-0.01). RHI predicted worse CogState One Back Test scores (β, 0.02; 95% CI, -0.01 to 0.05). There were RHI × TBI interaction effects on several neuropsychological subtests, and participants who had a history of both RHI and TBI with LOC had the greatest depression symptoms and worse cognition. CONCLUSIONS: RHI and TBI independently contributed to worse mid- to later-life neuropsychiatric and cognitive functioning.
OBJECTIVE: To test the hypothesis that repetitive head impacts (RHIs), like those from contact sport play and traumatic brain injury (TBI) have long-term neuropsychiatric and cognitive consequences, we compared middle-age and older adult participants who reported a history of RHI and/or TBI with those without this history on measures of depression and cognition. METHODS: This cross-sectional study included 13,323 individuals (mean age, 61.95; 72.5% female) from the Brain Health Registry who completed online assessments, including the Ohio State University TBI Identification Method, the Geriatric Depression Scale (GDS-15), and the CogState Brief Battery and Lumos Labs NeuroCognitive Performance Tests. Inverse propensity-weighted linear regressions accounting for age, sex, race/ethnicity, and education tested the effects of RHI and TBI compared to a non-RHI/TBI group. RESULTS: A total of 725 participants reported RHI exposure (mostly contact sport play and abuse) and 7,277 reported TBI (n = 2,604 with loss of consciousness [LOC]). RHI (β, 1.24; 95% CI, 0.36-2.12), TBI without LOC (β, 0.43; 95% CI, 0.31-0.54), and TBI with LOC (β, 0.75; 95% CI, 0.59-0.91) corresponded to higher GDS-15 scores. While TBI with LOC had the most neuropsychological associations, TBI without LOC had a negative effect on CogState Identification (β, 0.004; 95% CI, 0.001-0.01) and CogState One Back Test (β, 0.004; 95% CI, 0.0002-0.01). RHI predicted worse CogState One Back Test scores (β, 0.02; 95% CI, -0.01 to 0.05). There were RHI × TBI interaction effects on several neuropsychological subtests, and participants who had a history of both RHI and TBI with LOC had the greatest depression symptoms and worse cognition. CONCLUSIONS: RHI and TBI independently contributed to worse mid- to later-life neuropsychiatric and cognitive functioning.
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