scholarly journals Integration of Biomarkers Into a Signature Profile of Persistent Traumatic Brain Injury Involving Autoimmune Processes Following Water Hammer Injury From Repetitive Head Impacts

2018 ◽  
Vol 13 ◽  
pp. 117727191880821 ◽  
Author(s):  
Steven Kornguth ◽  
Neal Rutledge
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Responses ◽  
Vascular Malformations ◽  
Water Hammer ◽  
Host Factors ◽  
Time Interval ◽  
Head Impacts ◽  
Autoimmune Processes ◽  
Biochemical Analyses

Objectives: To assemble an algorithm that will describe a “Signature” predictive of an individual’s vulnerability to persistent traumatic brain injury (TBI) Subjects and Methods: Studies of athletes and warriors who are subjected to repeated head impacts with rapid acceleration/deceleration forces are used to assist in the diagnosis and management of TBI-affected individuals. Data from multiple areas, including clinical, anatomical, magnetic resonance imaging, cognitive function, and biochemical analyses, are integrated to provide a Signature of persistent TBI. Results: Studies to date indicate that susceptibility to TBI results from an interaction between host genetic and structural vulnerability factors and force and torque of impact on the head and torso. The host factors include molecular markers affecting immune and inflammatory responses to stress/insult as well as anatomical features such as the degree of transcortical fiber projections and vascular malformations. The host response to forceful impact includes the release of intracellular neural proteins and nucleic acids into the cerebrospinal fluid and vascular compartment as well as mobilization of cytokines and macrophages into the central nervous system with subsequent activation of microglia and inflammatory responses including autoimmune processes. Maximum impact to the base of the sulci via a “water hammer effect” is consistent with the localization of microvascular and inflammatory responses in the affected brain region. Conclusions: An assessment of an individuals’ predisposition to persistent TBI with delayed cognitive deficits and behavioral changes requires an understanding of host vulnerability (genetic factors and brain structure) and external stressors (force and torque of impact as well as repetitive head injury and time interval between impacts). An algorithm that has utility in predicting vulnerability to TBI will include qualitative and quantitative measures of the host factors weighted against post impact markers of neural injury. Implementation of the resulting “Signature” of vulnerability at early stages of injury will help inform athletes and warriors, along with commanders and management, of the risk/benefit approaches that will markedly diminish health care costs to the nation and suffering to this population. This report attempts to define a strategy to create such an algorithm.

Time Interval Between Traumatic Brain Injury And Post Traumatic Epilepsy

2013 ◽  
Vol 21 (2) ◽  
pp. 222-228
Author(s):  
Daniel Garbin Di Luca ◽  
Glenda Corrêa Borges de Lacerda
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
First Year ◽  
Time Interval ◽  
Partial Seizures ◽  
Complex Partial Seizures ◽  
Post Traumatic ◽  
Faster Development ◽  
Post Traumatic Epilepsy ◽  
Traumatic Epilepsy

Introduction. The estimated time interval in which an individual can develop Post Traumatic Epilepsy (PTE) after a traumatic brain injury (TBI) is not clear. Objective. To assess the possible influence of the clinical features in the time interval between TBI and PTE develop­ment. Method. We analyzed retrospectively 400 medical records from a tertiary Brazilian hospital. We selected and reevaluated 50 patients and data was confronted with the time between TBI and PTE devel­opment by a Kaplan-Meier survival analysis. A Cox-hazard regression was also conducted to define the characteristics that could be involved in the latent period of the PTE development. Results. Patients devel­oped PTE especially in the first year (56%). We found a tendency of a faster development of PTE in patients older than 24 years (P<0.0001) and in men (P=0.03). Complex partial seizures evolving to generalized seizures were predominant in patients after moderate (37.7%) and severe (48.8%) TBIs, and simple partial seizures evolving to general­ized seizures in mild TBIs (45.5%). Conclusions. Our data suggest that the first year after a TBI is the most critical period for PTE de­velopment and those males older than 24 years could have a faster development of PTE.

scholarly journals Predictive Factors of Kinematics in Traumatic Brain Injury from Head Impacts Based on Statistical Interpretation

2021 ◽  
Author(s):  
Xianghao Zhan ◽  
Yiheng Li ◽  
Yuzhe Liu ◽  
August G. Domel ◽  
Hossein Vahid Alizadeh ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Predictive Factors ◽  
Statistical Interpretation ◽  
Head Impacts

scholarly journals The HMGB1-RAGE axis mediates traumatic brain injury–induced pulmonary dysfunction in lung transplantation

2014 ◽  
Vol 6 (252) ◽  
pp. 252ra124-252ra124 ◽  
Author(s):  
Daniel J. Weber ◽  
Adam S. A. Gracon ◽  
Matthew S. Ripsch ◽  
Amanda J. Fisher ◽  
Bo M. Cheon ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Acute Lung Injury ◽  
Brain Injury ◽  
Lung Injury ◽  
Lung Transplantation ◽  
Inflammatory Responses ◽  
Pulmonary Dysfunction ◽  
Wild Type ◽  
Hmgb1 Protein ◽  
Lung Dysfunction

Traumatic brain injury (TBI) results in systemic inflammatory responses that affect the lung. This is especially critical in the setting of lung transplantation, where more than half of donor allografts are obtained postmortem from individuals with TBI. The mechanism by which TBI causes pulmonary dysfunction remains unclear but may involve the interaction of high-mobility group box-1 (HMGB1) protein with the receptor for advanced glycation end products (RAGE). To investigate the role of HMGB1 and RAGE in TBI-induced lung dysfunction, RAGE-sufficient (wild-type) or RAGE-deficient (RAGE−/−) C57BL/6 mice were subjected to TBI through controlled cortical impact and studied for cardiopulmonary injury. Compared to control animals, TBI induced systemic hypoxia, acute lung injury, pulmonary neutrophilia, and decreased compliance (a measure of the lungs’ ability to expand), all of which were attenuated in RAGE−/−mice. Neutralizing systemic HMGB1 induced by TBI reversed hypoxia and improved lung compliance. Compared to wild-type donors, lungs from RAGE−/−TBI donors did not develop acute lung injury after transplantation. In a study of clinical transplantation, elevated systemic HMGB1 in donors correlated with impaired systemic oxygenation of the donor lung before transplantation and predicted impaired oxygenation after transplantation. These data suggest that the HMGB1-RAGE axis plays a role in the mechanism by which TBI induces lung dysfunction and that targeting this pathway before transplant may improve recipient outcomes after lung transplantation.

scholarly journals Efficacy of Minocycline in Neural Stem Cells Proliferation after Traumatic Brain Injury

2020 ◽  
Vol 8 (A) ◽  
pp. 59-64
Author(s):  
R. R. Suzy Indharty ◽  
Iskandar Japardi ◽  
Andre M. P. Siahaan ◽  
Steven Tandean ◽  
Michael Lumintang Loe
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cells ◽  
Brain Injury ◽  
Neural Stem Cells ◽  
Inflammatory Responses ◽  
Closed Head Injury ◽  
Related Factor ◽  
Sprague Dawley ◽  
Proliferation Capacity ◽  
Cell Counts

BACKGROUND: Neuroinflammation is an important secondary injury mechanism that contributes to neurological impairments after traumatic brain injury (TBI). There is a robust evidence that neuroinflammation will diminish neurogenesis after TBI. Therefore, strategies to attenuate the inflammatory responses are potential to increase neurogenesis following TBI. Minocycline, a second-generation tetracycline antibiotic derivate, has potent anti-inflammatory effect by reducing microglial activation and suppressing some pro-inflammatory cytokines. AIM: The aim of this study is to investigate if minocycline could enhance neurogenesis after TBI. METHODS: Thirty Sprague Dawley rats were randomized into three treatments group, i.e., sham-operated controls, closed head injury (CHI), and CHI with minocycline. We used the modified Feeney’s weight-drop model for making CHI. For the treatment group, we gave minocycline per oral (50 mg/kg) twice daily for the first 2 days followed by 25 mg/kg once daily for 3 consecutive days. Animals were sacrificed on day 5. To assess the proliferation capacity of neural stem cells (NSC), we performed immunohistochemistry staining with SOX2, brain-derived neurotropic factor (BDNF), and NFR. Cell counts were carried out using light microscope with 1000 times magnification in 20 high-power fields. RESULTS: SOX2, NF-E2-related factor 2 (NRF-2), and BDNF were upregulated in the CHI group compared to the sham-operated group (p < 0.05). NRF-2, BDNF, and SOX2 were upregulated also significantly in the CHI+ minocycline group compared to the sham-operated group and the CHI group (p < 0.05). CONCLUSION: Minocycline increased the proliferation capacity of NSC.

scholarly journals Factors Affecting Traumatic Brain Injury Outcome Among Patients Treated for Head Injury at Surgical Side, in Nekemte Referral Hospital, Oromia, Ethiopia.

2020 ◽  
Vol 1 (2) ◽  
pp. 1-13
Author(s):  
Mitiku Getachew Kumara ◽  
Miresa Banti Dhugasa
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Conservative Management ◽  
Referral Hospital ◽  
Time Interval ◽  
Secondary Brain Injury ◽  
Major Public Health Problem ◽  
Delayed Presentation ◽  
Unfavourable Outcome

Background Traumatic brain injury is an expanding major public health problem and the leading cause of death of the young and productive part of the world’s population. Research is mainly done in high-income countries where only a small proportion of the worldwide fatalities occur. Only few studies have examined prognostic factors of traumatic brain injury outcome in developing countries including Ethiopia. This study was aimed at defining the peculiar demographic and other associated factors of traumatic brain injury (TBI) outcome among patients treated for head injury at Nekemte Referral Hospital. Objective The main purpose of this study was to describe the magnitude of TBI outcome and assess factors associated with unfavourable outcome of TBI among patients treated for head injury at the surgical side in Nekemte Referral Hospital from July 8, 2016 to July 7, 2018. Methods A retrospective cross-sectional document review was conducted among TBI patients treated for head injury from July 8, 2016 to July 7, 2018 at Nekemte Referral Hospital. Data were collected using a pre-tested data collection format. Data analysis was done using SPSS version 20. Descriptive statistics were computed and association between the dependent and independent variables were assessed by using logistic regression. Odds ratios with 95% confidence interval were computed. Significant association was declared when the p value was <0.05. Results In this study, out of 378 cases 95 (25.1%) were discharged with unfavourable outcome of which 37(9.8%) were neurologic deficits and 58 were deaths giving overall mortality rate of 15.3%. Patient age>60years (AOR: 15.13; 95%CI: 3.575-64.028), time interval from injury to treatment (AOR: 16.054; 95%CI: 5.832-44.194), low GCS (AOR: 18.224; 95%CI: 4.167, 79.695), conservative management (AOR: 20.774; 95%CI: 6.106-70.681), pupils abnormality (AOR: 9.078; 95%CI: AOR: 2.996-27.509) were associated with unfavourable outcome. Conclusions A quarter of patients treated for TBI at Nekemte Referral Hospital are discharged with unfavourable outcomes. Old age, delayed presentation to the hospital, low GCS, conservative management, and pupillary abnormality increase the odds of unfavourable outcome. Timely management of TBI before patients develop secondary brain injury and use of surgical intervention based on CT scan diagnosis will reduce the occurrence of unfavourable outcome.

scholarly journals Improving the translational potential of rodent models to study the behavioral and pathophysiological effects of repetitive mild traumatic brain injury

2018 ◽  
Vol 120 (1) ◽  
pp. 1-3
Author(s):  
Megan E. Huibregtse
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Outcome Measures ◽  
Mild Traumatic Brain Injury ◽  
Chronic Traumatic Encephalopathy ◽  
Rodent Models ◽  
Head Impacts ◽  
Repetitive Head Impacts ◽  
The Impact

Chronic traumatic encephalopathy (CTE) is thought to be caused by repetitive head impacts. Consequently, there is a need to develop rodent models to better understand the behavioral and pathophysiological changes of repetitive mild traumatic brain injury (rmTBI) and to determine the link between rmTBI and CTE. This Neuro Forum article reviews recent rodent rmTBI models, comparing the impact methods and outcome measures in terms of translational potential.

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