Identification of Factors in Moderate-Severe TBI Related to a Functional Decline in Cognition Decades After Injury.

OBJECTIVE: To investigate whether a functional decline in cognitive activities decades after moderate-to-severe traumatic brain injury (m-sTBI) might relate to injury features and/or lifetime health factors, some of which may emerge as consequences of the injury. DESIGN: Secondary analysis of the TBI Model Systems National Database, a prospective, multi-center, longitudinal study of patients with m-sTBI. SETTING: TBI Model Systems Centers. PARTICIPANTS: Included were 732 participants rated on the cognitive subscale of the Functional Independence Measure (FIM Cognitive), a metric for everyday cognitive skills, across 3 time points out to 20 years (visits at 2-, 10-, and 20-year follow-ups; N=732). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE(S): FIM Cognitive Scale. Injury characteristics such as timing and features pertaining to severity and health-related factors (eg, alcohol use, socioeconomic status) were examined to discriminate stable from declining participants on the FIM Cognitive Scale using logistic regression. RESULTS: At 20 years post-injury, there was a low base rate of FIM Cognitive decline (11%, n=78), with most being stable or having meaningful improvement (89%, n=654). Older age at injury, longer duration of post-traumatic amnesia, and presence of repetitive seizures were significant predictors of FIM Cognitive decline in the final model (area under the curve=0.75), while multiple health-related factors that can represent independent co-morbidities or possible consequences of injury were not. CONCLUSION(S): The strongest contributors to reported functional decline in cognitive activities later-in-life were related to acute characteristics of m-sTBI and experiencing post-traumatic seizures. Future studies are needed integrating functional with performance-based cognitive assessments to affirm conclusions and identify the timeline and trajectory of cognitive decline.

Neurocognitive outcomes of older National Football League retirees.

OBJECTIVE: Determine if head-injury exposure relates to later-in-life cognitive decline in older National Football League (NFL) retirees. METHOD: NFL retirees (aged 50+) with or without cognitive impairment underwent baseline (n = 53) and follow-up (n = 29; 13-59 months later) neuropsychological evaluations. Cognitively normal (CN) retirees (n = 26) were age- and education-matched to healthy controls (n = 26). Cognitively impaired (CI) retirees with mild cognitive impairment or dementia (n = 27) were matched to a clinical sample (CS) by age, sex, education, and diagnosis (n = 83). ANOVAs compared neuropsychological composites at baseline and over time between retirees and their matched groups. Regression models evaluated whether concussions, concussions with loss of consciousness (LOC), or games played predicted neuropsychological functioning. RESULTS: At baseline, CN retirees had slightly worse memory than controls (MCN retirees = 50.69, SECN retirees = 1.320; MHealthy controls = 57.08, SEHealthy controls = 1.345; p = 0.005). No other group diferences were observed, and head-injury exposure did not predict neurocognitive performance at baseline or over time. CONCLUSIONS: Head-injury exposure was not associated with later-in-life cognition, regardless of cognitive diagnosis. Some retirees may exhibit lower memory scores compared to age-matched peers, though this is of unclear clinical significance.

Traumatic brain injury alters neuropsychiatric symptomatology in all-cause dementia.

INTRODUCTION: Traumatic brain injury (TBI) may alter the course of neuropsychiatric symptom (NPS) onset during dementia development. The connection among TBI, NPS, and dementia progression is of increasing interest to researchers and clinicians. METHODS: Incidence of NPS was examined in participants with normal cognition who progressed to all-cause dementia based on whether TBI history was present (n = 130) or absent (n = 849). Survival analyses were used to examine NPS incidence across 7.6 ± 3.0 years of follow-up. RESULTS: Participants with TBI history had increased prevalence and incidence of apathy (44.7% vs 29.9%, P = .0062; HRadj. = 1.708, P = .0018) and motor disturbances (17.2% vs 9.5%, P = .0458; HRadj. = 2.023, P = .0168), controlling for demographics and type of dementia diagnosis. Earlier anxiety onset was associated with TBI (692 days prior to dementia diagnosis vs 161 days, P = .0265). DISCUSSION: History of TBI is associated with increased risk for and earlier onset of NPS in the trajectory of dementia development.

Clinical and neuropsychological profile of patients with dementia and chronic traumatic encephalopathy.

OBJECTIVE: To determine whether subjects with chronic traumatic encephalopathy (CTE) and dementia have distinct clinical features compared to subjects with pathologically confirmed Alzheimer's disease (AD). METHODS: Among 339 subjects assessed for CTE in the National Alzheimer's Coordinating Center dataset, 6 subjects with CTE and 25 subjects with AD neuropathologic change matched for age (±5 years) and sex were identified. All subjects had a clinical diagnosis of dementia. Neurological examination, neuropsychological testing and emotional/behavioural data were compared between CTE and AD subjects at the time of dementia diagnosis and last clinical visit near death. RESULTS: A history of traumatic brain injury with loss of consciousness (LOC) was reported in one CTE and one AD subject; information about injuries without LOC or multiple injuries was unavailable. CTE and AD subjects did not differ significantly at the time of diagnosis or last visit on the Unified Parkinson's Disease Rating Scale-Motor Exam, global measures of cognitive functioning (Mini-Mental State Exam and Clinical Dementia Rating Scale), emotional/behaviour symptoms as assessed with the Neuropsychiatric Inventory questionnaire or across neuropsychological measures. All CTE participants had co-occurring neuropathologic processes, including AD and most had TAR DNA-binding protein 43 (TDP-43) neuropathology. CONCLUSIONS: CTE pathology was rare in a large multicentre national dataset, and when present, was accompanied by AD and TDP-43 pathologies. CTE was not associated with a different clinical presentation from AD or with greater cognitive impairment or neurobehavioral symptoms. These findings suggest that CTE may not have a distinct clinical profile when other neuropathologic processes are coexistent with CTE pathology.

Associations of Race-Ethnicity and History of Traumatic Brain Injury With Age at Onset of Alzheimer's Disease.

OBJECTIVE: This study examined whether a history of traumatic brain injury (TBI) is associated with age at onset of Alzheimer's disease (AD) in three racial-ethnic groups. METHODS: Data from 7,577 non-Hispanic Caucasian, 792 African American, and 870 Hispanic participants with clinically diagnosed AD were obtained from the National Alzheimer's Coordinating Center. Participants were categorized by the presence or absence of self-reported remote history of TBI (>1 year before diagnosis of AD) with loss of consciousness (LOC) (TBI+) or no history of TBI with LOC (TBI-). Any group differences in education; sex; APOE ε4 alleles; family history of dementia; or history of depression, stroke, hypertension, hypercholesterolemia, and diabetes were included in analyses of covariance comparing clinician-estimated age at AD symptom onset for the TBI+ and TBI- groups. RESULTS: AD onset occurred 2.3 years earlier for non-Hispanic Caucasians (F=30.49, df=1, 7,572, p<0.001) and 3.4 years earlier for African Americans (F=5.17, df=1, 772, p=0.023) in the TBI+ group. In the Hispanic cohort, females in the TBI+ group had AD onset 5.6 years earlier, compared with females in the TBI- group (F=6.96, df=1, 865, p=0.008); little difference in age at AD onset was observed for Hispanic males with and without a TBI history. CONCLUSIONS: A history of TBI with LOC was associated with AD onset 2-3 years earlier in non-Hispanic Caucasians and African Americans and an onset nearly 6 years earlier in Hispanic females; no association was observed in Hispanic males. Further work in underserved populations is needed to understand possible underlying mechanisms for these differences.

Mild Cognitive Impairment in Retired Professional Football Players With a History of Mild Traumatic Brain Injury: A Pilot Investigation.

BACKGROUND: Traumatic brain injury (TBI) is a known risk factor for neurodegenerative dementias such as Alzheimer disease (AD); however, the potential risk of mild cases of TBI, such as concussions, remains unclear. OBJECTIVE: To explore whether a small sample of retired professional athletes with a diagnosis of mild cognitive impairment (MCI)-the prodromal stage of AD-and a history of multiple mild TBIs exhibit greater neuropsychological impairment than age-matched nonathletes with MCI and no history of TBI. METHOD: Ten retired National Football League players diagnosed with MCI and reporting multiple mild TBIs, and 10 nonathletes, also diagnosed with MCI but with no history of TBI, completed a standard neurologic examination and neuropsychological testing. Independent samples t tests were conducted to examine differences in neuropsychological performance between the two groups. RESULTS: The retired athletes with a history of mild TBI obtained generally similar scores to the nonathlete controls on measures of verbal learning and memory, verbal fluency, and processing speed. However, the retired athletes scored lower than the controls on tests of confrontation naming and speeded visual attention. CONCLUSION: Retired athletes with MCI and a history of mild TBI demonstrated similar neuropsychological profiles as nonathlete controls despite lower scores on measures of confrontation naming and speeded visual attention. These findings suggest that a history of multiple mild TBIs does not significantly alter the overall neuropsychological profile of individuals with MCI; confirmation of this will require longitudinal research with larger sample sizes.

Neuropsychological functioning in ageing retired NFL players: a critical review.

Recent discovery of chronic traumatic encephalopathy in former National Football League (NFL) players has led to a surge of papers investigating cognitive functioning in these former athletes. This critical review of the literature focused on the neuropsychological functioning in these ageing athletes, and included 22 articles published between 2013 and 2019, of which 13 reported on neuroradiological imaging and four focused on dose-response relationships of repetitive head injury on cognitive outcomes. Four studies suggest higher prevalence of MCI and neurodegenerative disease among NFL retirees, although a quantifiable risk and prevalence of cognitive impairment and dementia in these players remains unknown. Decreased verbal memory has been found in some players across multiple studies, though with unknown clinical significance due to small sample sizes, unreported effect sizes, and absence of longitudinal data. Studies investigating a dose-response relationship between cognitive decline and head injury have generated mixed findings utilizing various measures of head injury exposure. Neuroradiological findings are inconsistent, but suggest that some NFL players may be at greater risk for reduced white matter integrity. Future research is needed to understand the relationship between sports-related concussions and the risk of long-term cognitive decline and neurodegenerative disease in ageing NFL players.

History of traumatic brain injury interferes with accurate diagnosis of Alzheimer's dementia: a nation-wide case-control study.

Traumatic brain injury (TBI) and Alzheimer's disease (AD) bear a complex relationship, potentially increasing risk of one another reciprocally. However, recent evidence suggests post-TBI dementia exists as a distinct neurodegenerative syndrome, confounding AD diagnostic accuracy in clinical settings. This investigation sought to evaluate TBI's impact on the accuracy of clinician-diagnosed AD using gold standard neuropathological criteria. In this preliminary analysis, data were acquired from the National Alzheimer's Coordinating Centre (NACC), which aggregates clinical and neuropathologic information from Alzheimer's disease centres across the United States. Modified National Institute on Aging-Reagan criteria were applied to confirm AD by neuropathology. Among participants with clinician-diagnosed AD, TBI history was associated with misdiagnosis (false positives) (OR = 1.351 [95% CI: 1.091-1.674], p = 0.006). Among participants without clinician-diagnosed AD, TBI history was not associated with false negatives. TBI moderates AD diagnostic accuracy. Possible AD misdiagnosis can mislead patients, influence treatment decisions, and confound research study designs. Further work examining the influence of TBI on dementia diagnosis is warranted.

Risk factors for earlier dementia onset in autopsy-confirmed Alzheimer's disease, mixed Alzheimer's with Lewy bodies, and pure Lewy body disease.

INTRODUCTION: Clinical Alzheimer's disease (AD) and dementia with Lewy bodies often have mixed AD and Lewy pathology, making it difficult to delineate risk factors. METHODS: Six risk factors for earlier dementia onset due to autopsy-confirmed AD (n = 647), mixed AD and Lewy body disease (AD + LBD; n = 221), and LBD (n = 63) were entered into multiple linear regressions using data from the National Alzheimer's Coordinating Center. RESULTS: In AD and AD + LBD, male sex and apolipoprotein E (APOE) ɛ4 alleles each predicted a 2- to 3-year-earlier onset and depression predicted a 3-year-earlier onset. In LBD, higher education predicted earlier onset and depression predicted a 5.5-year-earlier onset. DISCUSSION: Male sex and APOE ɛ4 alleles increase risk for earlier dementia onset in AD but not LBD. Depression increases risk for earlier dementia onset in AD, LBD, and AD + LBD, but evaluating the course, treatment, and severity is needed in future studies.

Neurodegenerative Dementias After Traumatic Brain Injury.

Traumatic brain injury (TBI) is often considered to be a risk factor for the later development of neurodegenerative conditions, but some findings do not support a link. Differences in research methods, clinical samples, and limitations encountered when assessing and documenting TBI details likely contribute to the mixed reports in the literature. Despite some variability in findings, a review of the literature does provide support for the notion that TBI appears to be associated with earlier onset of some neurodegenerative disorders, although clearly not everyone with a TBI appears to be at an increased risk. Whereas a mechanistic link remains unknown, TBI has been found to initiate an accumulation of pathological processes related to several neurodegenerative disorders. The authors propose a hypothetical model that relates TBI to the development of pathological burden overlapping with some neurodegenerative conditions, in which onset of cognitive/behavioral impairments is hastened in some individuals, but pathological processes stabilize afterward, resulting in a similar course of decline to individuals with dementia who do not have a history of TBI.

Traumatic brain injury history is associated with earlier age of onset of frontotemporal dementia.

OBJECTIVE: We retrospectively examined whether a history of traumatic brain injury (TBI) is associated with an earlier age of symptom onset and diagnosis in a large sample of patients with behavioural variant frontotemporal dementia (bvFTD). METHODS: Data on patients with bvFTD (n=678) were obtained from the National Alzheimer's Coordinating Center Uniform Data Set. TBI was categorised based on reported lifetime history of TBI with loss of consciousness (LOC) but no chronic deficits occurring more than 1 year prior to diagnosis of bvFTD. Analysis of covariance (ANCOVA) was used to determine if clinician-estimated age of symptom onset and age at diagnosis of bvFTD differed between those who reported a history of TBI with LOC (TBI+) and those who did not (TBI-). RESULTS: Controlling for sex, the TBI+ bvFTD group had an age of symptom onset and age of diagnosis that was on average 2.8 and 3.2 years earlier (p<0.01) than the TBI- bvFTD group. CONCLUSIONS: TBI history with LOC occurring more than 1 year prior to diagnosis is associated with an earlier age of symptom onset and diagnosis in patients with bvFTD. TBI may be related to the underlying neurodegenerative processes in bvFTD, but the implications of age at time of injury, severity and repetitive injuries remain unclear.

Optimal neurocognitive, personality and behavioral measures for assessing impulsivity in cocaine dependence.

BACKGROUND: Impulsivity may underlie the poor treatment retention and high relapse rates observed in cocaine-dependent persons. However, observed differences in measures of impulsivity between cocaine-dependent and healthy control participants often do not reach clinical significance, suggesting that the clinical relevance of these differences may be limited. OBJECTIVES: To examine which measures of impulsivity (i.e. self-report impulsivity, self-report personality, neurocognitive testing) best distinguish cocaine-dependent and healthy control participants (i.e. showing differences at least 1.5 standard deviations [SD] from controls). Optimal measures were considered to demonstrate sufficient classification accuracy. METHODS: Sixty-five recently abstinent cocaine-dependent and 25 healthy control participants were assessed using select neurocognitive tests and self-report questionnaires including the NEO Personality Inventory-Revised (NEO-PI-R), Temperament and Character Inventory (TCI), Barratt Impulsiveness Scale (BIS-11a), and the Frontal Systems Behavior Scale (FrSBe). RESULTS: When corrected for years of education and gender, neurocognitive measures did not demonstrate clinically significant differences between cocaine-dependent and control participants. The personality measures TCI Purposefulness and Congruent Second Nature and NEO-PI-R Impulsiveness, and the self-rating measures FrSBe Disinhibition and BIS-11 Motor Impulsivity and Total successfully identified clinically meaningful elevations in impulsivity within cocaine-dependent participants (>1.5 SDs from controls). Furthermore, these measures achieved 84-93% accuracy in discriminating cocaine-dependent from control participants. CONCLUSION: Clinically significant neurocognitive impairment in cocaine-dependent participants was not observed in this sample. As the BIS-11 or FrSBe are brief to administer, accurate, and have been shown to predict treatment retention and relapse, these measures appear to be optimal, relative to the personality measures, for examining trait impulsivity in cocaine dependence.

Traumatic Brain Injury Characteristics Are Not Related to Neurocognitive Decline in Older Adults: A Nationwide Longitudinal Cohort Study.

OBJECTIVE: Evaluate whether traumatic brain injury (TBI) characteristics, age of injury, or recency of injury predicts the course of neurocognitive decline and/or increases conversion rates to mild cognitive impairment (MCI) or dementia. METHODS: Data were obtained from the National Alzheimer's Coordinating Center for participants 50-85 years old with 3-5 visits from 2015 to 2022, with or without TBI history (TBI+ = 508; TBI- = 2,382). Groups were stratified by self-reported TBI history (i.e., single TBI without loss of consciousness [LOC], single TBI with LOC, multiple TBI without LOC, and multiple TBI with LOC), age of most recent TBI, and recency of TBI. Mixed linear models compared neuropsychological composite trajectories (executive functioning/attention/speed, language, memory, and global), co-varying for age, gender, education, apolipoprotein E4 status, race/ethnicity, and baseline diagnosis (normal aging n = 1,720, MCI n = 749, or dementia n = 417). Logistic binary regression examined MCI/dementia conversion rates. RESULTS: There was a slightly higher frequency of MCI/dementia in those with multiple TBIs (50% to 60% with and without LOC, compared to 39% with no TBI) at baseline, but longitudinal trajectories were similar. TBI history, age of injury, or recency of injury did not impact neurocognitive trajectories or conversion rates to MCI/dementia (all p's > .01). CONCLUSIONS: TBI history, regardless of injury characteristics, age of injury, or recency of injury, did not worsen neurocognitive decline or MCI/dementia conversion. Additional longitudinal research in more diverse cohorts with a wider range of TBI severity is needed to evaluate the specific factors and possible mechanisms in which TBI may increase dementia risk.

A Critical Review of Noninvasive Brain Stimulation Technologies in Alzheimer's Dementia and Primary Progressive Aphasia.

Multiple pharmacologic agents now have been approved in the United States and other countries as treatment to slow disease and clinical progression for Alzheimer's disease. Given these treatments have not been proven to lessen the cognitive deficits already manifested in the Alzheimer's Clinical Syndrome (ACS), and none are aimed for another debilitating dementia syndrome identified as primary progressive aphasia (PPA), there is an urgent need for new, safe, tolerable, and efficacious treatments to mitigate the cognitive deficits experienced in ACS and PPA. Noninvasive brain stimulation has shown promise for enhancing cognitive functioning, and there has been interest in its potential therapeutic value in ACS and PPA. This review critically examines the evidence of five technologies in ACS and PPA: transcranial direct current stimulation (tDCS), transcranial alternating current stimulation (tACS), transcranial random noise stimulation (tRNS), repetitive transcranial magnetic stimulation (rTMS), and noninvasive vagus nerve stimulation (nVNS). Many randomized controlled trials of tDCS and rTMS report positive treatment effects on cognition in ACS and PPA that persist out to at least 8 weeks, whereas there are few trials for tACS and none for tRNS and nVNS. However, most positive trials did not identify clinically meaningful changes, underscoring that clinical efficacy has yet to be established in ACS and PPA. Much is still to be learned about noninvasive brain stimulation in ACS and PPA, and shifting the focus to prioritize clinical significance in addition to statistical significance in trials could yield greater success in understanding its potential cognitive effects and optimal parameters.

Verbal retrieval deficits due to traumatic brain injury are associated with changes in event related potentials during a Go-NoGo task.

OBJECTIVE: Verbal retrieval (VR) deficits often occur after traumatic brain injury (TBI), but the mechanisms remain unclear. We examined how event-related potentials (ERPs) during a Go-NoGo task were associated with VR deficits. METHODS: Sixty veterans with a history of TBI underwent a neuropsychological battery and a Go-NoGo task with concurrent EEG recording. We compared task performance and ERP measures (N2, P3) between those with and those without persistent injury-related VR deficits. We then used generalized linear modeling to examine the relationship between ERP measures and scores on measures of executive function and processing speed. RESULTS: Go-NoGo task performance was comparable between the groups. Those with VR deficits had larger N2 amplitude in NoGo than in Go conditions. In participants with VR deficits, larger NoGo N2/P3 amplitude predicted faster processing speed. Furthermore, larger P3 amplitude and shorter P3 latency of the difference wave (NoGo - Go) predicted faster processing speed in those with VR deficits. CONCLUSIONS: Despite no difference in Go-NoGo task performance, ERP amplitude and latency measures associated with cognitive control during Go-NoGo distinguished TBI individuals with VR deficits from those without. SIGNIFICANCE: This study furthers our understanding of VR deficits in TBI and implicates potential application of ERP measures in monitoring and treating such deficits.

Blood Markers in Relation to a History of Traumatic Brain Injury Across Stages of Cognitive Impairment in a Diverse Cohort.

BACKGROUND: Traumatic brain injury (TBI) has been linked to multiple pathophysiological processes that could increase risk for Alzheimer's disease and related dementias (ADRD). However, the impact of prior TBI on blood biomarkers for ADRD remains unknown. OBJECTIVE: Using cross-sectional data, we assessed whether a history of TBI influences serum biomarkers in a diverse cohort (approximately 50% Hispanic) with normal cognition, mild cognitive impairment, or dementia. METHODS: Levels of glial fibrillary acidic protein (GFAP), neurofilament light (NFL), total tau (T-tau), and ubiquitin carboxy-terminal hydrolase-L1 (UCHL1) were measured for participants across the cognitive spectrum. Participants were categorized based on presence and absence of a history of TBI with loss of consciousness, and study samples were derived through case-control matching. Multivariable general linear models compared concentrations of biomarkers in relation to a history of TBI and smoothing splines modelled biomarkers non-linearly in the cognitively impaired groups as a function of time since symptom onset. RESULTS: Each biomarker was higher across stages of cognitive impairment, characterized by clinical diagnosis and Mini-Mental State Examination performance, but these associations were not influenced by a history of TBI. However, modelling biomarkers in relation to duration of cognitive symptoms for ADRD showed differences by history of TBI, with only GFAP and UCHL1 being elevated. CONCLUSIONS: Serum GFAP, NFL, T-tau, and UCHL1 were higher across stages of cognitive impairment in this diverse clinical cohort, regardless of TBI history, though longitudinal investigation of the timing, order, and trajectory of the biomarkers in relation to prior TBI is warranted.

No association between age beginning tackle football, or years played and neurocognitive performance later-in-life among older National Football League retirees.

OBJECTIVE: In a retrospective cohort, we evaluated whether age beginning tackle football (ABTF) and more total years of playing football (TYPF) were associated with worse later-in-life neuropsychological change among older retired National Football League (NFL) players. METHOD: Participants were 19 older NFL retirees aged 54-79, including 12 who returned for follow-up evaluation 15-51 months later. Mixed-linear models evaluated the association between ABTF/TYFP and baseline neuropsychological composite scores (executive functioning/attention/speed, language, memory), and neuropsychological composites over time. RESULTS: ABTF and TYPF were not significantly associated with neuropsychological composites at baseline or over time (all p's > .05). There were no significant differences in neuropsychological performance between those ABTF <12 and ≥ 12 years old (all p's ≥ .475) or between those with TYPF <19 or ≥ 19 years played (median split; all p's ≥ .208). CONCLUSIONS: Preliminary findings suggest that ABTF and TYPF does not worsen neurocognitive decline later-in-life among older NFL retirees.

History of traumatic brain injury does not alter course of neurocognitive decline in older adults with and without cognitive impairment.

OBJECTIVE: Traumatic brain injury (TBI) history is associated with dementia risk, but it is unclear whether TBI history significantly hastens neurocognitive decline in older adults. METHOD: Data were derived from the National Alzheimer's Coordinating Center (NACC) data set. Participants with a history of TBI (TBI +; n = 1,467) were matched to individuals without a history of TBI (TBI-; n = 1,467) based on age (50-97, M = 71.61, SD = 8.40), sex, education, race, ethnicity, cognitive diagnosis, functional decline, number of Apolipoprotein ε4 (APOE ε4) alleles, and number of annual visits (3-6). Mixed linear models were used to assess longitudinal neuropsychological test composite scores of executive functioning/attention/speed, language, and memory in TBI + and TBI- participants. Interactions between TBI and demographics, APOE ε4 status, and cognitive diagnosis were also examined. RESULTS: Longitudinal neuropsychological functioning did not differ between TBI groups (p's > .001). There was a significant three-way interaction (age, TBI history, time) in language (F[20, 5750.1] = 3.133, p < .001) and memory performance (F[20, 6580.8] = 3.386, p < .001), but post hoc analyses revealed TBI history was not driving this relationship (all p's > .096). No significant interactions were observed between TBI history and sex, education, race/ethnicity, number of APOE ε4 alleles, or cognitive diagnosis (p's > .001). CONCLUSIONS: Findings suggest TBI history, regardless of demographic factors, APOE ε4 status, or cognitive diagnosis, does not alter the course of neurocognitive functioning later-in-life in older adults with or without cognitive impairment. Future clinicopathological longitudinal studies that well-characterize head injuries and the associated clinical course are needed to help clarify the mechanism in which TBI may increase dementia risk. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Early vs. delayed evaluation and persisting concussion symptoms during recovery in adults.

Objective: Persisting concussion symptoms may adversely affect return to work and functioning in daily activities. This study compared adults who were initially evaluated < 30 days versus those evaluated ≥ 30 days following a concussion at a specialty concussion clinic to determine if delayed initial evaluation is associated with persisting symptoms during recovery. Method: Participants (N = 205) 18 years of age and older who sustained a concussion and presented to a North Texas Concussion Registry (ConTex) clinic were evaluated at two time points: initial clinical visit and three-month follow-up. Participants provided medical history, injury related information, and completed the Sport Concussion Assessment Tool-5 Symptom Evaluation, Generalized Anxiety Disorder 7-item scale (GAD-7), and Patient Health Questionnaire (PHQ-8). Participants were divided into two groups: early and delayed evaluation (±30 days post injury). Results: Number and severity of concussion symptoms were similar between both groups at their initial clinical visit. However, linear regression models showed that a delayed clinical evaluation was associated with a greater number and severity of concussion symptoms along with greater aggravation of symptoms from physical and cognitive activity at three-month follow-up. Conclusions: Individuals who sought care at specialty concussion clinics regardless of previous care 30 or more days following their injury reported more serious persisting concussion symptoms at three month follow-up than those who sought care sooner. Education to improve adults' recognition of concussions when they occur and obtaining earlier clinical evaluation may represent important opportunities in promoting better recovery and reducing persisting concussion symptoms.