Project description:IntroductionTraumatic Brain Injury (TBI) accounts for millions of hospitalizations and deaths worldwide. Aerobic exercise is an easily implementable, non-pharmacological intervention to treat TBI, however, there are no clear guidelines for how to best implement aerobic exercise treatment for TBI survivors across age and injury severity.MethodsWe conducted a PRISMA-ScR to examine research on exercise interventions following TBI in children, youth and adults, spanning mild to severe TBI. Three electronic databases (PubMed, PsycInfo, and Web of Science) were searched systematically by two authors, using keywords delineated from "Traumatic Brain Injury," "Aerobic Exercise," and "Intervention."ResultsOf the 415 papers originally identified from the search terms, 54 papers met the inclusion criteria and were included in this review. The papers were first grouped by participants' injury severity, and subdivided based on age at intervention, and time since injury where appropriate.DiscussionAerobic exercise is a promising intervention for adolescent and adult TBI survivors, regardless of injury severity. However, research examining the benefits of post-injury aerobic exercise for children and older adults is lacking.
Project description:The temporal course of microglial inflammation-related gene expression was defined uding nanostring platform at acute, subacute, and chronic time points in a pre-clinical TBI model.
Project description:Traumatic brain injury (TBI) can lead to significant neuropsychiatric problems and neurodegenerative pathologies, which develop and persist years after injury. Neuroinflammatory processes evolve over this same period. Therefore, we aimed to determine the contribution of microglia to neuropathology at acute (1-day post-injury; dpi), subacute (7 dpi), and chronic (30 dpi) time-points. Microglia were depleted with PLX5622, a CSF1R antagonist, prior to midline fluid percussion injury in male mice and cortical neuropathology/inflammation was assessed using a neuropathology mRNA panel. NanoString Neuropathology gene expression panel was used to quantify expression from RNA microdissected from the mouse cortex.
Project description:The neuroinflammatory response to traumatic brain injury (TBI) is critical to both neurotoxicity and neuroprotection, and has been proposed as a potentially modifiable driver of secondary injury in animal and human studies. Attempts to broadly target immune activation have been unsuccessful in improving outcomes, in part because the precise cellular and molecular mechanisms driving injury and outcome at acute, subacute, and chronic time points after TBI remain poorly defined. Microglia play a critical role in neuroinflammation and their persistent activation may contribute to long-term functional deficits. Activated microglia are characterized by morphological transformation and transcriptomic changes associated with specific inflammatory states. We analyzed the temporal course of changes in inflammatory genes of microglia isolated from injured brains at 2, 14, and 60 days after controlled cortical impact (CCI) in mice, a well-established model of focal cerebral contusion. We identified a time dependent, injury-associated change in the microglial gene expression profile toward a reduced ability to sense tissue damage, perform housekeeping, and maintain homeostasis in the early stages following CCI, with recovery and transition to a specialized inflammatory state over time. This later state starts at 14 days post-injury and is characterized by a biphasic pattern of IFNγ, IL-4, and IL-10 gene expression changes, with concurrent proinflammatory and anti-inflammatory gene changes. Our transcriptomic data sets are an important step to understand microglial role in TBI pathogenesis at the molecular level and identify common pathways that affect outcome. More studies to evaluate gene expression at the single cell level and focusing on subacute and chronic timepoint are warranted.
Project description:ObjectiveTo examine cognitive function in individuals with traumatic brain injury (TBI) prior to and after participation in an aerobic exercise training program.DesignPre-post intervention study.SettingMedical research center.ParticipantsVolunteer sample of individuals (N=7) (age, 33.3±7.9y) with chronic nonpenetrating TBI (injury severity: 3=mild, 4=moderate; time since most current injury: 4.0±5.5y) who were ambulatory.InterventionTwelve weeks of supervised vigorous aerobic exercise training performed 3 times a week for 30 minutes on a treadmill.Main outcome measuresCognitive function was assessed using the Trail Making Test Part A (TMT-A), Trail Making Test Part B (TMT-B), and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Sleep quality and depression were measured with the Pittsburgh Sleep Quality Index (PSQI) and Beck Depression Inventory, version 2 (BDI-II). Indices of cardiorespiratory fitness were used to examine the relation between improvements in cognitive function and cardiorespiratory fitness.ResultsAfter training, improvements in cognitive function were observed with greater scores on the TMT-A (10.3±6.8; P=.007), TMT-B (9.6±7.0; P=.011), and RBANS total scale (13.3±9.3; P=.009). No changes were observed in measures of the PSQI and BDI-II. The magnitude of cognitive improvements was also strongly related to the gains in cardiorespiratory fitness.ConclusionsThese findings suggest that vigorous aerobic exercise training may improve specific aspects of cognitive function in individuals with TBI and cardiorespiratory fitness gains may be a determinant of these improvements.
Project description:BackgroundPatients with traumatic brain injury (TBI) usually have mood and anxiety symptoms secondary to their brain injury. Exercise may be a cost-effective intervention for the regulation of the affective responses of this population. However, there are no studies evaluating the effects of exercise or the optimal intensity of exercise for this clinical group.MethodsTwelve male patients with moderate or severe TBI [mean age of 31.83 and SD of 9.53] and 12 age- and gender-matched healthy volunteers [mean age of 30.58 and SD of 9.53] participated in two sessions of exercise of high and moderate-intensity. Anxiety and mood was evaluated, and subjective assessment of experience pre- and post-exercise was assessed. A mixed between and within-subjects general linear model (GLM) analysis was conducted to compare groups [TBI, control] over condition [baseline, session 1, session 2] allowing for group by condition interaction to be determined. Planned comparisons were also conducted to test study hypotheses.ResultsAlthough no group by condition interaction was observed, planned comparisons indicated that baseline differences between patients and controls in anxiety (Cohens' d = 1.80), tension (d = 1.31), depression (d = 1.18), anger (d = 1.08), confusion (d = 1.70), psychological distress (d = 1.28), and physical symptoms (d = 1.42) disappear after one session of exercise, independently of the intensity of exercise.ConclusionA single-section of exercise, regardless of exercise intensity, had a positive effect on the affective responses of patients with TBI both by increasing positive valence feelings and decreasing negative ones. Exercise can be an easily accessible intervention that may alleviate depressive symptoms related to brain injury.
Project description:OBJECTIVE:To examine cardiorespiratory fitness in individuals with traumatic brain injury (TBI), before and following participation in a supervised 12-week aerobic exercise training program. METHODS:Ten subjects with nonpenetrating TBI (TBI severity: mild, 50%; moderate, 40%; severe, 10%; time since injury [mean ± SD]: 6.6 ± 6.8 years) performed exercise training on a treadmill 3 times a week for 30 minutes at vigorous intensity (70%-80% of heart rate reserve). All subjects completed a cardiopulmonary exercise test, with pulmonary gas exchange measured and a questionnaire related to fatigue (Fatigue Severity Scale) at baseline and following exercise training. RESULTS:After training, increases (P < .01) in peak oxygen consumption ((Equation is included in full-text article.); +3.1 ± 2.4 mL/min/kg), time to volitional fatigue (+1.4 ± 0.8 minutes), and peak work rate (+59 ± 43 W) were observed. At the anaerobic threshold, (Equation is included in full-text article.)(+3.6 ± 2.1 mL/kg/min), treadmill time (+1.8 ± 1.1 minutes), and work rate (+37 ± 39 W) were higher (P < .01) following exercise training. Subjects also reported significantly lower (P < .05) Fatigue Severity Scale composite scores (-0.9 ± 1.3) following exercise training. CONCLUSION:These findings suggest that individuals with TBI may benefit from participation in vigorous aerobic exercise training with improved cardiorespiratory fitness and diminished fatigue.
Project description:Physical activity and exercise are important adjuncts to medical treatment for overall health in individuals with traumatic brain injury (TBI); however, many individuals do not partake in the recommended weekly exercise. The objective of this study was to investigate the barriers to exercise after TBI and determine whether these barriers varied by age. The sample was 172 adults with moderate to severe TBI who completed Barriers to Physical Exercise and Disability (B-PED) survey. Lack of interest, motivation, and energy as well as cost, lack of counseling on exercise by a physician, not having home equipment, and being too lazy were reported as barriers to exercise by all age groups. Those aged 35 to 54-years-old were more likely to report that cost, lack of transportation, having health concerns, not knowing where to exercise, and fear of leaving the home as barriers to exercise than those aged 18 to 34-years-old or 55-years-old and older. Overall, adults with TBI report multiple barriers to exercise, and these barriers vary by age.
Project description:Most patients who die after traumatic brain injury (TBI) show evidence of ischemic brain damage. Nevertheless, it has proven difficult to demonstrate cerebral ischemia in TBI patients. After TBI, both global and localized changes in cerebral blood flow (CBF) are observed, depending on the extent of diffuse brain swelling and the size and location of contusions and hematoma. These changes vary considerably over time, with most TBI patients showing reduced CBF during the first 12 hours after injury, then hyperperfusion, and in some patients vasospasms before CBF eventually normalizes. This apparent neurovascular uncoupling has been ascribed to mitochondrial dysfunction, hindered oxygen diffusion into tissue, or microthrombosis. Capillary compression by astrocytic endfeet swelling is observed in biopsies acquired from TBI patients. In animal models, elevated intracranial pressure compresses capillaries, causing redistribution of capillary flows into patterns argued to cause functional shunting of oxygenated blood through the capillary bed. We used a biophysical model of oxygen transport in tissue to examine how capillary flow disturbances may contribute to the profound changes in CBF after TBI. The analysis suggests that elevated capillary transit time heterogeneity can cause critical reductions in oxygen availability in the absence of 'classic' ischemia. We discuss diagnostic and therapeutic consequences of these predictions.