Traumatic brain injury (TBI) affects over 48 million people worldwide each year. Suicide is common in TBI, and there are several known contributing factors, including severe TBI, depression, alcohol use, and male sex. Impulsivity, or the tendency to act quickly with little thought, may be an early predictor of suicidality following TBI. The purpose of this study was to evaluate the risk of suicidality in patients with a prior history of impulsivity following a traumatic brain injury (TBI). Using de-identified electronic health records from the TriNetX United States Collaborative Network with Natural Language Processing, three cohorts were generated: the impulsivity TBI cohort (I+TBI+) included subjects with a diagnosis of impulsivity before a diagnosis of TBI; the no impulsivity TBI cohort (I-TBI+) included patients with TBI but no impulsivity; the impulsivity no TBI cohort (I+TBI-) included patients with impulsivity but TBI. Two analyses were conducted, including analysis 1 (impulsivity TBI vs. no impulsivity TBI) and analysis 2 (impulsivity TBI vs. impulsivity no TBI). Patients were 1:1 propensity score matched by age, sex, race, ethnicity, psychiatric diagnoses, and antidepressant use. Outcomes included a diagnosis of self-harm, suicidal ideation, or a suicide attempt within one year after the index event. The all-time incidence of each outcome was assessed across different age categories. The chi-square test (categorical variables) and t-test (numerical variables) were used to assess for differences between groups. A total of 1,292,776 TBI patients were identified in the study. After 1:1 propensity score-matching, there were 20,694 patients (mean [SD] age, 48.1 [21.8]; 8,424 females [40.7%]) with impulsivity and TBI (I+TBI+), 1,272,082 patients (mean [SD] age, 46.0 [23.1]; 562,705 females [44.2%]) with TBI alone (I-TBI+), and 90,669 patients (mean [SD] age, 43.7 [22.6]; 45,188 females [49.8%]) with impulsivity alone (I+TBI-). Within the first year after a TBI, patients with impulsivity were more likely to exhibit self-harm (P < 0.001), suicidal ideation (P < 0.001) or a suicide attempt (P < 0.001). Compared to TBI patients without impulsivity, those with impulsivity had a four-fold increase in the incidence of self-harm (2.81% vs. 0.63%), an eight-fold increase in suicidal ideation (52.42% vs. 6.41%), and a twenty-one-fold increase in suicide attempts (32.02% vs. 1.50%). This study suggests that impulsivity diagnosed before a TBI may increase the risk of post-traumatic suicidality, with a four-fold increased risk of self-harm, an eight-fold increased risk of suicidal ideation and a twenty-one-fold increased risk of suicide attempts. This characterizes a group of at-risk individuals who may benefit from early psychiatric support and targeted interventions following a TBI.

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A precise understanding of the latency to post-traumatic epilepsy (PTE) following a traumatic brain injury (TBI) is necessary for optimal patient care. This precision is currently lacking despite a surprising number of available data sources that could address this pressing need. Following guidance from the Cochrane Collaboration and Joanna Briggs Institute, we conduct a systematic review to address the research questions: What is the cumulative incidence of PTE following mild TBI (mTBI; concussion), and what is the distribution of the latency to onset? We designed a comprehensive search of medical databases and gray literature sources. Citations will be screened on both abstract and full-text levels, independently and in duplicate. Studies will be evaluated for risk of bias independently and in duplicate using published instruments specific to incidence/prevalence studies. Data will be abstracted independently and in duplicate using piloted extraction forms. Disagreements will be resolved by consensus or third-party adjudication. Evidence synthesis will involve pairwise and individual participant data meta-analysis with heterogeneity explored via a set of predetermined subgroups. The robustness of the findings will be subjected to sensitivity analyses based on the risk of bias, outlier studies, and mTBI definitional criteria. The overall certainty in the estimates will be reported using GRADE (Grading of Recommendations, Assessment, Development, and Evaluations). This protocol presents an innovative and impactful approach to build on the growing body of knowledge surrounding post-mTBI PTE. Through a precise understanding of the latency period, this study can contribute to early detection, tailored interventions, and improved outcomes, leading to a substantial impact on patient care and quality of life.

The International Mission on Prognosis and Analysis of Clinical Trials in Traumatic Brain Injury (IMPACT) model is a widely recognized prognostic model applied after traumatic brain injury (TBI). However, it was developed with patient cohorts that may not reflect modern practice patterns in North America. We analyzed data from two sources: the placebo arm of the phase II double-blinded, multicenter, randomized controlled trial Prehospital Tranexamic Acid for TBI (TXA) cohort and an observational cohort with similar inclusion/exclusion criteria (Predictors of Low-risk Phenotypes after Traumatic Brain Injury Incorporating Proteomic Biomarker Signatures [PROTIPS] cohort). All three versions of the IMPACT model-core, extended, and laboratory-were evaluated for 6-month mortality (Glasgow Outcome Scale Extended [GOSE] = 1) and unfavorable outcomes (GOSE = 1-4). Calibration (intercept and slope) and discrimination (area under the receiver operating characteristic curve [ROC-AUC]) were used to assess model performance. We then compared three model updating methods-recalibration in the large, logistic recalibration, and coefficient update-with the best update method determined by likelihood ratio tests. In our calibration analysis, recalibration improved both intercepts and slopes, indicating more accurate predicted probabilities when recalibration was done. Discriminative performance of the IMPACT models, measured by AUC, showed mortality prediction ROCs between 0.61 and 0.82 for the TXA cohort, with the coefficient updated Lab model achieving the highest at 0.84. Unfavorable outcomes had lower AUCs, ranging from 0.60 to 0.79. Similarly, in the PROTIPS cohort, AUCs for mortality ranged from 0.75 to 0.82, with the coefficient updated Lab model also showing superior performance (AUC 0.84). Unfavorable outcomes in this cohort presented AUCs from 0.67 to 0.73, consistently lower than mortality predictions. The closed testing procedure using likelihood ratio tests consistently identified the coefficient update model as superior, outperforming the original and recalibrated models across all cohorts. In our comprehensive evaluation of the IMPACT model, the coefficient updated models were the best performing across all cohorts through a structured closed testing procedure. Thus, standardization of model updating procedures is needed to reproducibly determine the best performing versions of IMPACT that reflect the specific characteristics of a dataset.

Few studies have examined long-term mortality following traumatic brain injury (TBI) in a military population. This is a secondary analysis of a prospective, longitudinal study that examines long-term mortality (up to 10 years) post-TBI, including analyses of life expectancy, causes of death and risk factors for death in service members and veterans (SM/V) who survived the acute TBI and inpatient rehabilitation. Among 922 participants in the study, the mortality rate was 8.3% following discharge from inpatient rehabilitation. The mean age of death was 54.5 years, with death occurring on average 3.2 years after injury, and with an average 7-year life expectancy reduction. SM/V with TBI were nearly 4 times more likely to die compared with the US general population. Leading causes of death were external causes of injury, circulatory disease, and respiratory disorders. Also notable were deaths due to late effects of TBI itself and suicide. Falls were a significant mechanism of injury for those who died. Those who died were also more likely to be older at injury, unemployed, non-active duty status, not currently married, and had longer post-traumatic amnesia, longer rehabilitation stays, worse independence and disability scores at rehabilitation discharge, and a history of mental health issues prior to injury. These findings indicate that higher disability and less social supportive infrastructure are associated with higher mortality. Our investigation into the vulnerabilities underlying premature mortality and into the major causes of death may help target future prevention, surveillance, and monitoring interventions.

Brain fluid clearance by pathways including the recently described paravascular glymphatic system is a critical homeostatic mechanism by which metabolic products, toxins, and other wastes are removed from the brain. Brain fluid clearance may be especially important after traumatic brain injury (TBI), when blood, neuronal debris, inflammatory cells, and other substances can be released and/or deposited. Using a non-invasive dynamic positron emission tomography (PET) method that models the rate at which an intravenously injected radiolabeled molecule (in this case 11C-flumazenil) is cleared from ventricular cerebrospinal fluid (CSF), we estimated the overall efficiency of brain fluid clearance in humans who had experienced complicated-mild or moderate TBI 3-6 months before neuroimaging (n = 7) as compared to healthy controls (n = 9). While there was no significant difference in ventricular clearance between TBI subjects and controls, there was a significant group difference in dependence of ventricular clearance upon tracer delivery/blood flow to the ventricles. Specifically, in controls, ventricular clearance was highly, linearly dependent upon blood flow to the ventricle, but this relation was disrupted in TBI subjects. When accounting for blood flow and group-specific alterations in blood flow, ventricular clearance was slightly (non-significantly) increased in TBI subjects as compared to controls. Current results contrast with past studies showing reduced glymphatic function after TBI and are consistent with possible differential effects of TBI on glymphatic versus non-glymphatic clearance mechanisms. Further study using multi-modal methods capable of assessing and disentangling blood flow and different aspects of fluid clearance is needed to clarify clearance alterations after TBI.

Children of parents with traumatic brain injury (TBI) are more likely to develop psychiatric disorders. This association is usually attributed to TBI-induced changes in parents\' personality and families\' social environment. We tested the hypothesis that offspring of young adult male rats with TBI develop neurodevelopmental abnormalities in the absence of direct social contact with sires. Male Sprague-Dawley rats (F0 generation) in the TBI group underwent moderate TBI via a midline fluid percussion injury that involved craniectomy under sevoflurane (SEVO) anesthesia for 40 min on post-natal Day 60 (P60), while F0 rats in the control group were placed in a new cage, one per cage, for the equivalent time duration. A subset of F0 rats was sacrificed on P66 to assess acute changes in hypothalamic-pituitary-adrenal (HPA) axis and inflammation markers. The remaining F0 males were mated with naive females on P90 to generate offspring (F1 generation). The F0 males and F1 males and females were sequentially evaluated in the elevated plus maze, for pre-pulse inhibition of acoustic startle, in the Morris water maze, and for resting and stress levels of serum corticosterone starting on ∼P105 (F0) and ∼P60 (F1), followed by tissue collection for further analyses. Acutely, the F0 TBI males had messenger RNA (mRNA) transcripts altered to support an increased hypothalamic and hippocampal Na+-K+-Cl- (Slc12a2) Cl- importer / K+-2Cl- (Slc12a5) Cl- exporter ratio and decreased hippocampal glucocorticoid receptors (Nr3c1), as well as increased serum levels of corticosterone, interleukin-1β (IL-1β), and biomarkers of activated hippocampal microglia and astrocytes. Long-term, F0 TBI rats exhibited increased corticosterone concentrations at rest and under stress, anxiety-like behavior, impaired sensory-motor gating, and impaired spatial memory. These abnormalities were underpinned by reduced mRNA levels of hypothalamic and hippocampal mineralocorticoid receptors (Nr3c2), hippocampal Nr3c1, and hypothalamic brain-derived neurotrophic factor (Bdnf), as well as elevated serum levels of IL-1β, and biomarkers of activated hippocampal microglia and astrocytes. F1 male offspring of TBI sires exhibited abnormalities in all behavioral tests, while their F1 female counterparts had abnormal pre-pulse inhibition responses only. F1 male offspring of TBI sires also had reduced mRNA levels of hippocampal Nr3c1 and Nr3c2, as well as hypothalamic and hippocampal Bdnf, whereas increases in inflammatory markers were more profound in F1 females. These findings suggest that offspring of sires with a history of a moderate TBI that involved craniectomy under SEVO anesthesia for 40 min, develop sex-dependent neurobehavioral abnormalities in the absence of direct social interaction between the sire and the offspring.

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