Browsing by Subject "Brain Injuries, Traumatic"
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Item Effects of Aerobic Exercise Training on Carotid Arterial Stiffness and Brain Health in Traumatic Brain Injury(2020-05-01T05:00:00.000Z) Le, Tran B.; Ding, Kan; Zhang, Rong; Bell, Kathleen R.; Tomoto, TsubasaBACKGROUND: Vascular dysfunction and hypoperfusion in the brain are common after traumatic brain injury (TBI). The brain is perfused by elastic central arteries that decrease in compliance with age, leading to decreased ability to dampen hemodynamic pulsatility and decreased continuous blood flow in cerebral vasculature. Aerobic exercise improves cardiorespiratory fitness, health status, quality of life, and cognitive function as well as decrease mortality in normal adults. In this regard, physical activity, particularly aerobic exercise training (AET), may have favorable effects on TBI-related vascular and cerebral blood flow (CBF) changes. However, knowledge gaps regarding the effects of chronic TBI on vascular function still exist. Furthermore, little is known about the effect of AET on carotid arterial stiffness and CBF in patients with TBI with pre-existing brain injury. OBJECTIVE: We hypothesized that TBI patients may continue to suffer from vascular impairments at the chronic stage and may benefit from aerobic exercise with improvements in cardiorespiratory fitness, decrease in carotid arterial stiffness, and improved brain health. METHODS: Twenty-three participants with a history of mild to severe TBI and twenty-five age- gender-fitness level-matched participants with no history of TBI were recruited for the normal control group (non-TBI). All participants were 18-65 years old and have a sedentary lifestyle. The groups were divided into young (19-44 years old) and middle-aged (45-63 years old) for further analysis. Carotid arterial compliance was measured using common carotid artery echography and applanation tonometry. Transcranial Doppler was used to measure the cerebral blood flow velocities. Carotid arterial compliance was calculated from the carotid diameters and blood pressures. Seventeen of the TBI survivors (age: 48±13 years, 10 women) with persistent neurological symptoms 6-60 months after initial injury were randomized to 3-month moderate-intensity AET or control stretching program (SAT) and completed the interventions. Among them, 10 sustained mild TBI and 7 had moderate to severe TBI. Cardiorespiratory fitness was assessed by peak oxygen uptake (VO2peak) using a modified Astrand-Saltin treadmill protocol. Carotid arterial compliance was measured as measured. Neuropsychological function was assessed using the NIH Toolbox cognition battery and the PROMIS assessment. RESULTS: In the cross-sectional portion of the study, hemodynamic parameters indicate that the TBI group had higher brachial blood pressure (116.4 ± 10.4 vs. 109.8 ± 9.3 mmHg, p < 0.05). and carotid systolic blood pressure (113.0 ± 11.0 vs. 102.8 ± 10.6 mmHg, p < 0.05) than the non-TBI groups at rest. Arterial compliance was significantly lower in the TBI vs. non-TBI group (0.101 + 0.025 vs. 0.120 + 0.029 mm2/mmHg, p < 0.05). Additionally, cerebrovascular resistance was significantly higher in the TBI vs. non-TBI group (0.168 + 0.0332 vs. 0.145 + 0.0290 mmHg/mL/min, p < 0.05). Ten participants were randomized to AET group and seven to stretching group. No age, gender, or VO2peak differences were noted at baseline between AET and stretching groups. The duration of the intervention was twelve weeks. Although no statistically significant changes were observed following the intervention, different trends were observed. VO2peak increased by 7% in AET yet decreased by 4% in stretching; arterial compliance increased by 12 % in AET and decreased by 2% in stretching; NIH Toolbox fluid composite score, which assessed adaptability to new experience, improved by 15% in AET and 9% in stretching; and the NIH Toolbox total composite score, which involves adaptability to new experiences as well as past knowledge and skills, improved by 7% in AET versus 4% in stretching. CONCLUSION: The results suggest that TBI is associated with increased blood pressure, which is consistent with existing literature. The elevated blood pressure potentially leads is associated with decreased arterial compliance and increased resistance in the cerebral vasculature. Previous literature suggests that decreased cerebral blood flow may be associated with the cognitive impairment in TBI patients. For the longitudinal portion of the study, the physiological measurements (includingVO2peak, arterial compliance, and pulsatility index) and cognitive measurements suggest the potential positive effect of AET on physiological and cognitive improvement in patients with TBI. Physical activity, both SAT and AET, can improve arterial compliance in patients with chronic TBI.Item Epidemiology of Traumatic Brain Injuries at a Major Government Hospital in Cambodia(2017-03-02) Peeters, Sophie Monique; Mihalic, Angela; Madden, Christopher; Gatson, JoshuaBACKGROUND: Traumatic brain injury (TBI) is a critical public health problem worldwide with a significant socioeconomic burden. While improved safety regulations in high-income countries have resulted in a decline in traffic-related TBI, the incidence of TBI in low-income countries is on the rise. We illustrate the trends and factors involved in TBI in a large Cambodian governmental hospital in Phnom Penh. Additionally, suggestions for improvement of the country's road traffic safety are discussed. METHODS: This is a cross-sectional study of all patients who presented with traumatic brain injury to Department of Neurosurgery at Preah Kossamak Hospital in Phnom Penh, Cambodia between November 2013 and March 2016. RESULTS: Traumatic brain injuries in Cambodia are on the rise. 34% occur during rush hour, 5 to 9pm, and 40% during the weekend. The vast majority (74%) is due to road traffic accidents, of which 81% are motorcycle related. Helmet wear remains low at 13% and recent alcohol use was reported as 38%. The most common diagnosis is skull fracture. The subdural to epidural hematoma ratio was 1:1.05. Lastly, in both subdural and epidural hematomas the frontal lobe was most commonly involved, with 60% of epidural hematomas associated with a lucid interval. CONCLUSIONS: Our study suggests prevention and management of TBIs can have a measurable public health impact in Cambodia. Initiative examples include helmet safety awareness campaigns, stricter penalties, improvement of pre-hospital care, and more efficient triage. High proportion of un-helmeted motorcycle accidents correlates with a rise in epidural hematomas.Item Increased Amyloid Deposition after TBI Correlates with Cognitive Deficits and Symptom Worsening(2016-01-19) Sherman, Matt; Gatson, Joshua; Stebbins, Cari; Kilianski, Joseph; Madden, Christopher; Wolf, Steven E.; Diaz-Arrastia, Ramon; Batjer, Hunt; Minei, JosephBACKGROUND: Traumatic brain injury (TBI) is a risk factor for Alzheimer's disease (AD). The primary objective of this case-series study was to conduct early 18F-AV-45 (florbetapir F18) positron emission tomography (PET) imaging in mild-to-moderate TBI subjects after injury to determine if amyloid plaque load predicts cognitive deficits. METHODS: Serial florbetapir F18 PET imaging was conducted in 7 individuals with a mild or moderate TBI (as indicated by their Glasgow Coma Scale [GCS] score between 13 and 15) at day 14 and at 12 months after injury. Of the 7 subjects that were tested, only one had a moderate TBI. Amyloid plaque levels were measured in the cerebral cortex of each individual. To screen for cognitive deficits, the symbol match test was administered at 12 months after TBI. RESULTS: At day 14 after injury, compared to healthy controls, the mild and moderate TBI subjects (N=7) had a 10% increase in amyloid plaque load within the cerebral cortex. When stratified by cognitive outcomes, at day 14 after injury, the subjects with poor outcomes (n=3) experienced a 20% and 13% increase in brain amyloid compared to healthy controls and TBI subjects with good outcomes, respectively. With respect to cognition, at 12 months after injury, the subjects with poor outcomes exhibited a negative correlation (r= -0.71) between amyloid plaque load and cognitive performance. Also, a positive correlation (r=+0.78) was detected between increased brain amyloid load and symptom scores at 12 months. CONCLUSIONS: Individuals with early, substantial increases in brain amyloid experience poor outcomes in the form of memory dysfunction and heightened symptoms (memory deficits, headaches, difficulty concentrating, etc.) at 12 months post-injury. Data presented here suggests that florbetapir F18 PET imaging may be a sensitive biomarker for predicting outcomes within the mild and moderate TBI population.Item Neuropsychological Profiles in Temporal Lobe Epilepsy With and Without a History of Traumatic Brain Injury(2018-07-25) Wadsworth, Hannah Elizabeth; Cullum, C. Munro; Lacritz, Laura H.; Hynan, Linda S.; Busch, Robyn; Ding, KanNeuropsychological deficits have long been observed in those with temporal lobe epilepsy (TLE). Language and verbal memory are often impaired in individuals with left TLE and visuospatial and visual memory can be impaired in patients with right TLE. Traumatic brain injury (TBI) is the most common known cause of epilepsy. Given the heterogeneous nature of TBI, neurocognitive deficits can vary after injury; however, difficulty in memory, attention, processing speed, and executive functioning are consistently observed. Even though these two neurological conditions are intertwined, very little is known about the combined effects on neurocognitive functioning. This study aimed to examine neuropsychological functioning in TLE patients with and without a history of TBI. It was predicted that those with a history of TBI would have greater deficits in attention, processing speed, and executive functioning than those without TBI. Binary logistic regression models were used to determine the value of an array of neuropsychological measures in differentiating those with and without TBI. Results suggested greater cognitive difficulties, particularly in executive functioning, in those with a history of TBI. Understanding that TLE patients with a TBI history could have greater cognitive impairments may assist with clinician interpretation of neuropsychological findings. Future research should expand on the current results to further describe differences in epilepsy populations with and without a history of TBI in a larger, more diverse sample, and with a greater number of individuals who completed semantic fluency and AVLT.Item Phosphatase Regulation of Mechanical Stress and Aging in C. elegans(2020-08-01T05:00:00.000Z) Egge, Nathan Chandler; Goldsmith, Elizabeth J.; Douglas, Peter; Mendell, Joshua T.; Terman, Jonathan R.; Joachimiak, LukaszStress and aging embody two related processes driving cellular dysfunction. In either case, environmental stimuli and genetically encoded regulatory mechanisms affect cellular homeostasis and influence adaptation. Phosphatases represent master regulators of stress signaling and modulate cellular responses and fate during stress and aging. Yet, physiologically relevant mechanisms by which these phosphatases are regulated or orchestrate stress response and lifespan are incompletely understood. Herein, I present two scenarios, mechanical trauma and intestinal aging, both of which involve regulation by phosphatases. Mechanical stimuli initiate adaptive signal transduction pathways, but exceeding cell tolerance for physical stress results in degeneration and death via unclear mechanisms. In the nematode C. elegans, I developed a model to study cellular degeneration in response to mechanical stress caused by blunt force trauma. I identified a dual-specificity MAPK phosphatase, VHP-1, as a stress-inducible modulator of neurodegeneration. VHP-1 regulates the transcriptional response to mechanical stress and itself is dually regulated by its target, KGB-1. KGB-1 both activates VHP-1 via a negative feedback loop and represses via inhibition of a deubiquitinase, MATH-33, affecting proteasomal degradation. Thus, I describe an uncharacterized stress response pathway in C. elegans and identify transcriptional and post-translational components comprising a feedback loop on Jun kinase and phosphatase activity. Like stress, aging challenges cell tolerances, instigating death upon inadequacy of homeostatic regulation. Intestinal cells form a vital barrier separating environment from organism. Age impairs intercellular interactions and the cells' capacity to tightly associate within tissues and form an effective barrier necessary for normal systemic function. In particular, the actin cytoskeleton represents a key determinant in maintaining tissue architecture; how age disrupts the actin cytoskeleton, and, in turn, promotes mortality remains unclear. Herein, I show that phosphorylation of ACT-5 compromises C. elegans intestinal barrier integrity and accelerates pathogenesis. Age-related loss of the heat shock transcription factor, HSF-1, disrupts the Jun kinase/Protein Phosphatase I equilibrium, increasing ACT-5 phosphorylation within a troponin-binding site. Phosphorylated ACT-5 accelerates decay of the intestinal terminal web and impairs cell junctions. Therefore, age-associated dysregulation of phosphatase/kinase activity contributes to intestinal dysmorphogenesis and organism death.Item Self-Reported Head Injury: Associated Risk in Mild Cognitive Impairment and Progression to Alzheimer Disease(2016-07-27) LoBue, Christian Barrett; Cullum, C. Munro; Woon, Fu Lye; Rossetti, Heidi; Hart, John, Jr.; Hynan, Linda S.Traumatic brain injury (TBI) has been associated with a higher risk for and earlier onset of neurodegenerative disorders, including Alzheimer disease (AD), but its mechanistic link is not well understood. TBI has been hypothesized to activate a progressive neurodegenerative process, accelerate an already present neurodegenerative disorder, or disrupt neuronal/cognitive reserve and interact with aging. Although previous research has investigated the link between TBI and dementia, little is known if TBI is also associated with development of mild cognitive impairment (MCI), a prodromal phase of AD, and progression from MCI to AD. This broad investigation consists of two studies devised to examine whether a history of TBI is a risk factor for MCI and progression from MCI to AD using a large, multicenter national database. The aim of Study 1 was to determine if a history of TBI with LOC was associated with an increased risk for and earlier onset of MCI. Results revealed that a history of TBI was associated with a 1.35 fold higher risk for a diagnosis of MCI, even after adjusting for well-known factors linked to cognitive decline. A history of TBI was also linked to a nearly 2 year earlier age of MCI diagnosis. Thus, a TBI history does appear to be associated with an earlier diagnosis of MCI and may be a risk factor for MCI. Study 2 was devised to investigate whether a history of TBI with LOC was associated with progression from MCI to AD. Results revealed that individuals with a history of TBI with LOC did not show faster progression from MCI to AD, higher annual rates of progression, or more rapid cognitive decline than those without a TBI history, suggesting that a history of TBI was not linked to progression from MCI to AD. This two-part investigation indicates that a history of TBI appears to be a risk factor for earlier development of MCI; however, once the neurodegenerative process for MCI to AD starts, a history of TBI appears unrelated to subsequent decline.Item [UT Southwestern Medical Center News](2007-10-03) Stafford, Erin PratherItem [UT Southwestern Medical Center News](2011-05-26) Rian, RussellItem [UT Southwestern Medical Center News](2009-06-29) Piloto, Connie; Thomason, ChariseItem [UT Southwestern Medical Center News](2011-03-30) Donihoo, Rachel