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Relevant bibliographies by topics / Traumatic brain injury

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Academic literature on the topic 'Traumatic brain injury'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 January 2025

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Journal articles on the topic "Traumatic brain injury"

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Adelson, P. David. "Pediatric Traumatic Brain Injury : Present and Future Considerations in Management(Traumatic Brain Injury: Recent Advances)." Japanese Journal of Neurosurgery 19, no. 3 (2010): 196–201. http://dx.doi.org/10.7887/jcns.19.196.

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Volovitzr, Ilan. "Neuropsychological Assessment of Traumatic Brain Injury." Neuroscience and Neurological Surgery 2, no. 2 (April 20, 2018): 01–02. http://dx.doi.org/10.31579/2578-8868/028.

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Kocamer Şahin, Şengül, Ufuk Gönültaş, and Bahadır Demir. "TRICOTILLLOMANIA SECONDARY TO TRAUMATIC BRAIN INJURY." PSYCHIATRIA DANUBINA 35, no. 3 (October 23, 2023): 430–32. http://dx.doi.org/10.24869/psyd.2023.430.

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Pal, Urvashi. "TRAUMATIC BRAIN INJURY AND ITS MANAGEMENT." Indian Journal of Health Care Medical & Pharmacy Practice 5, no. 1 (May 25, 2024): 134–43. http://dx.doi.org/10.59551/ijhmp/25832069/2024.5.1.170.

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A prevalent illness with a high morbidity and death rate is head injuries. Early detection and evacuation are crucial for serious cerebral hemorrhages in order to optimize the likelihood of independent recovery. It isthe primary cause of death for children and young people and a significant medical and socioeconomic issue. The Brain Trauma Foundation’s “Guidelines for the Management of this disease” are a major source of inspiration for critical care management of this injury. The primary goals are to maintain cerebral perfusion pressure (CPP), optimize cerebral oxygenation, and prevent and cure intracranial hypertension and secondary brain injuries. The care management of (TBI) will be covered in this review, with particular attention paid to monitoring, preventing and minimizing subsequent brain insults, and optimizing cerebral oxygenation and CPP. The influences of worrying mind damage can be profound and lengthy-lasting, affecting all aspects ofsomeone’slife. However, with suitable assist, rehabilitation, and adaptive techniques, many individuals with TBI are capable of lead pleasant and significant lives.

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Griffin, Allison D., L. Christine Turtzo, Gunjan Y. Parikh, Alexander Tolpygo, Zachary Lodato, Anita D. Moses, Govind Nair, et al. "Traumatic microbleeds suggest vascular injury and predict disability in traumatic brain injury." Brain 142, no. 11 (October 14, 2019): 3550–64. http://dx.doi.org/10.1093/brain/awz290.

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Abstract Traumatic microbleeds are small foci of hypointensity seen on T2*-weighted MRI in patients following head trauma that have previously been considered a marker of axonal injury. The linear appearance and location of some traumatic microbleeds suggests a vascular origin. The aims of this study were to: (i) identify and characterize traumatic microbleeds in patients with acute traumatic brain injury; (ii) determine whether appearance of traumatic microbleeds predict clinical outcome; and (iii) describe the pathology underlying traumatic microbleeds in an index patient. Patients presenting to the emergency department following acute head trauma who received a head CT were enrolled within 48 h of injury and received a research MRI. Disability was defined using Glasgow Outcome Scale-Extended ≤6 at follow-up. All magnetic resonance images were interpreted prospectively and were used for subsequent analysis of traumatic microbleeds. Lesions on T2* MRI were stratified based on ‘linear’ streak-like or ‘punctate’ petechial-appearing traumatic microbleeds. The brain of an enrolled subject imaged acutely was procured following death for evaluation of traumatic microbleeds using MRI targeted pathology methods. Of the 439 patients enrolled over 78 months, 31% (134/439) had evidence of punctate and/or linear traumatic microbleeds on MRI. Severity of injury, mechanism of injury, and CT findings were associated with traumatic microbleeds on MRI. The presence of traumatic microbleeds was an independent predictor of disability (P < 0.05; odds ratio = 2.5). No differences were found between patients with punctate versus linear appearing microbleeds. Post-mortem imaging and histology revealed traumatic microbleed co-localization with iron-laden macrophages, predominately seen in perivascular space. Evidence of axonal injury was not observed in co-localized histopathological sections. Traumatic microbleeds were prevalent in the population studied and predictive of worse outcome. The source of traumatic microbleed signal on MRI appeared to be iron-laden macrophages in the perivascular space tracking a network of injured vessels. While axonal injury in association with traumatic microbleeds cannot be excluded, recognizing traumatic microbleeds as a form of traumatic vascular injury may aid in identifying patients who could benefit from new therapies targeting the injured vasculature and secondary injury to parenchyma.

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Fatima, Tahreem, Muhammad Irshad, Muhammad Rizwan Sarwar, Rahmatullah Salah, Abdul Ghaffoor, and Freshta Asekzai. "Effect of Traumatic Brain Injury on Serum Magnesium." International Journal of Science and Research (IJSR) 11, no. 8 (August 5, 2022): 266–69. http://dx.doi.org/10.21275/sr22801002707.

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Savelieff, Masha G., and Eva L. Feldman. "Traumatic Brain Injury." Neurology 96, no. 8 (January 6, 2021): 357–58. http://dx.doi.org/10.1212/wnl.0000000000011455.

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McNair, Norma D. "TRAUMATIC BRAIN INJURY." Nursing Clinics of North America 34, no. 3 (September 1999): 637–59. http://dx.doi.org/10.1016/s0029-6465(22)02411-2.

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Fernoagă, Cristina, and Mihai Cătălin Cereaciuchin. "Traumatic brain injury." Practica Veterinara.ro 2, no. 36 (2022): 22. http://dx.doi.org/10.26416/pv.36.2.2022.6432.

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Nelasari, Diamond, Astri Sumandari, and Ridha Sasmitha Ajiningrum. "Traumatic Brain Injury." KESANS : International Journal of Health and Science 1, no. 4 (January 21, 2022): 357–67. http://dx.doi.org/10.54543/kesans.v1i4.34.

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Traumatic brain injury (TBI) is an injury to the brain that is non-degenerative and non-congenital but is caused by external mechanical forces that can cause a decrease in consciousness and temporary or permanent disturbances in cognitive, physical, and psychosocial functions. The latest data from the CDC in 2014 there were as many as 2.87 million people in the world suffered head injuries. Certain segments of society that are at high risk for TBI include young people, low-income individuals, unmarried individuals, members of ethnic minority groups, male gender, urban dwellers, substance abusers, and people with previous TBI. Keywords: Head Trauma, Traumatic Brain Injury, Radiology

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Dissertations / Theses on the topic "Traumatic brain injury"

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Force, Lisa Marie. "Traumatic brain injury and acidosis /." view abstract or download text of file, 2006. http://hdl.handle.net/1794/3913.

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Singh, Rajiv K. "Depression after traumatic brain injury." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18730/.

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Background Depression is known to be common after traumatic brain injury (TBI) and associated with worse functional and psychosocial outcomes. However, there remains considerable uncertainty over the exact prevalence of the condition. Aims The aim of this study was to accurately assess the prevalence of post TBI depression and its changes over a period of one year. The associated demographic and injury features were also examined for possible association with risk of depression in the hope that those with higher susceptibility to depression may be identified. Methods The study population was a prospective cohort of TBI admissions to a teaching hospital emergency department over a two year period. Minimal exclusions were applied in order to recruit a representative TBI population who were then assessed in a specialist brain injury clinic at ten weeks and at one year post injury. Demographic and injury features were recorded to establish links with risk of depression which was recorded with a HADS (Hospital Anxiety and Depression Scale). Results Over a two year period, 774 individuals were recruited of whom 690 attended one year follow-up and 38 had died. Only 6% of the cohort was lost to follow-up after one year. The prevalence of depression at ten weeks was 56.3% [95% CI 52.8-59.8] and at one year 41.2% [95% CI 37.6-44.9] A multivariable analysis identified the independent predictors of depression; at ten weeks these were TBI severity, abnormal CT scan, past psychiatric history, alcohol intoxication at the time of injury, female gender and non-white ethnicity. At one year the independent predictors were; abnormal CT scan, past psychiatric history, alcohol intoxication at the time of injury and female gender. TBI severity was no longer significant. Features such as injury aetiology, social isolation, age, length of stay and medical comorbidity were not associated with depression risk. All other outcome measures in the study, including psychosocial function, symptom severity and global overall outcome showed very high correlations with depression. Discussion The prevalence of depression is very high after TBI and associated with a number of injury features. While the prevalence drops over a year it still remains considerably elevated. There is also evidence that features related to the injury itself, such as TBI severity, become less significant in long term outcome compared to the initial period. It is possible that other psychosocial features such as personality and coping mechanisms are more important in determining long term outcome than injury features such as severity and aetiology. Some population features have been identified that may allow targeting of susceptible populations for intervention. The close correlations between all 4 outcome measures including depression suggest that they might be measuring a similar construct of emotional distress. Future work will seek to reassess the prevalence of depression at three or five years as well as associated features, re-examining the relationship between various outcomes and use of interventions and treatments, especially in targeting at risk individuals.

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Perel, Pablo Andraes. "Prognosis in traumatic brain injury." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2009. http://researchonline.lshtm.ac.uk/1635515/.

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Introduction: The general purpose of this thesis was to study prognosis in traumatic brain injury (TBI) patients, with the aim of providing useful and practical information in clinical practice and clinical research. The specific objectives were: to develop and validate practical prognostic models for TBI patients and to assess the validity of the Modified Oxford Handicap Scale (mOHS) for predicting disability at six months. Methods: A survey was first conducted to understand the importance of prognostic information among physicians. A systematic review of prognostic models for TBI patients was then carried out. Prognostic models were developed using data from a cohort of 10,008 TBI patients (CRASH trial) and validated in a cohort of 8,509 TBI patients (IMPACT study). Two focus groups and a survey were conducted to develop a paper-based prognostic score card. The correlation between the mOHS and the Glasgow Outcome Scale (GOS) was assessed, the validity of different mOHS dichotomies was assessed, and the discriminative ability of the mOHS to predict GOS was evaluated. Results: Doctors considered prognostic information to be very important in the clinical management of TBI patients, and believed that an accurate prognostic model would change their current clinical practice. Many prognostic models for TBI have been published, but they have many methodological flaws which limit their validity. Valid prognostic models for patients from high income countries and low & middle income .countries were developed and made available as a web calculator, and as a paper based score card. The mOHS was strongly correlated with and was predictive of GOS at six months. Conclusion: The prognostic models developed are valid and practical to use in the clinical setting. The association between mOHS and GOS suggest that the mOHS could be used for interim analysis in randomised clinical trials in TBI patients, for dealing with loss to follow-up, or could be used as simple tool to inform patients and relatives about their prognosis at hospital discharge.

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Rowe, Rachel K. "POST-TRAUMATIC SLEEP FOLLOWING DIFFUSE TRAUMATIC BRAIN INJURY." UKnowledge, 2013. http://uknowledge.uky.edu/neurobio_etds/7.

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Traumatic brain injury (TBI) is a major cause of death and disability throughout the world with few pharmacological treatments available for individuals who suffer from neurological morbidities associated with TBI. Cellular and molecular pathological processes initiated at the time of injury develop into neurological impairments, with chronic sleep disorders (insomnia, hypersomnolence) being among the somatic, cognitive and emotional neurological impairments. Immediately post-injury, TBI patients report excessive daytime sleepiness, however, discordant opinions suggest that individuals should not be allowed to sleep or should be frequently awoken following brain injury. To provide adequate medical care, it is imperative to understand the role of acute post-traumatic sleep on the recovery of neurological function after TBI. The aim of this thesis was to examine post-traumatic sleep after experimental TBI, defined as an increase in sleep during the first hours post-injury. In these studies, we non-invasively measured sleep activity following diffuse brain injury induced by midline fluid percussion injury to examine the architecture of post-traumatic sleep in mice. We detected significant injury-induced increases in acute sleep for six hours regardless of injury severity or time of day injury occurred. We found concurrent increases in cortical levels of the sleep promoting inflammatory cytokine interleukin 1-beta. We extended the timeline of post-injury sleep recording and found increases in post-traumatic sleep are distinctly acute with no changes in chronic sleep following diffuse TBI. Further, we investigated if post-traumatic sleep was beneficial to neurological outcome after brain-injury by disrupting post-traumatic sleep. Disruption of post-traumatic sleep did not worsen functional outcome (neuromotor, sensorimotor, cognition) at one week after diffuse TBI. With sufferers of TBI not always seeking medical attention, our final studies investigated over-the-counter analgesics and their effect on post-traumatic sleep and functional outcome. Acute administration of analgesics with varying anti-inflammatory properties had little effect on post-traumatic sleep and functional outcome. Overall, these studies demonstrated translational potential and suggest sleep after a concussion is part of the natural recovery from injury. While disrupting sleep does not worsen outcome, it is in no way beneficial to recovery. Additionally, a single analgesic dose for pain management following concussion plays little role in short term outcome.

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Keller, Kristen Jo. "Challenges to Secondary Brain Injury Prevention in Severe Traumatic Brain Injury." Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/338712.

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BACKGROUND/AIMS: Inconsistency in the use of secondary brain injury prevention guidelines among US trauma centers after severe traumatic brain injury is prevalent in many literature sources. However, this phenomenon has not been thoroughly studied. The purpose of this DNP project is to identify the key barriers and challenges in compliance to the evidence-based guidelines for secondary brain injury prevention. DESIGN: An exploratory, emergent design was used to collect descriptive qualitative data through the use of a survey. SETTING: Six Phoenix Metropolitan Level 1 trauma centers. PARTICIPANTS: All survey participants who consented to survey completion, which had greater than six months of experience and directly worked with patients suffering from a severe TBI in the clinical setting. MEASUREMENTS: Participant demographics (work experience, area of work, job title), current awareness and use of Brain Trauma Foundation guidelines, and time duration for evidence based order set implementation. Narrative responses were also used to identify barriers to current use of the BTF guidelines and factors that may promote their use in the future. RESULTS: A total of 43 participants consented to the survey study, with completion by 35 participants. RNs (n=27), Physicians (n=2), NPs or PAs (n=5), with an average work experience of 6 to 14 years (42.86%). A total of n=22 (62%) of participants were unaware of the current BTF guidelines for severe TBI and only 25% (n=9) aware that their facility has a protocol based on the BTF guidelines for severe TBI, while 51% (n=18) were unsure if their facility had a protocol. Barriers were identified in narrative form and were consistent with awareness/education, provider congruence, communication, and order set/protocol process improvement. CONCLUSION: The understanding of current patient management for severe TBI based on the BTF guidelines is sporadic among the greater Phoenix area Level 1 trauma centers. Requiring proof of BTF guidelines compliance by the ACS at time of Level 1 certification may increase the consistent recommended use of the BTF guidelines for the care of severe TBIs.

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Al-Hasani, Omer Hussain. "Traumatic brain injury with particular reference to diffuse traumatic axonal injury subpopulations." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5569.

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Traumatic brain injury (TBI) remains an important cause of morbidity and mortality within society. TBI may result in both focal and diffuse brain injury. Diffuse traumatic axonal injury (TAI) is an important pathological substrate of TBI, and can be associated with a range of clinical states, ranging from concussion through to death, the clinical severity being associated with a number of factors related to the injury. A retrospective study was conducted using 406 cases with TBI, from the archive of the Academic Department of Pathology (Neuropathology) University of Edinburgh, during the period from1982 and 2005. This cohort was sequential and provided a unique description of the range of pathologies associated with fatal TBI within the Edinburgh catchment area. All the data was collected on a proforma and analysed to provide a description of the incidence in the injury patterns among the Edinburgh cohort. This cohort was then used to provide cases to try and critically assess the mechanisms of axonal injury in TBI. A study was undertaken to investigate TAI in an experimental model of non-impact head injury in a gyrencephalic mammalian model (piglet model) and in human autopsy materials using immunohistochemical analysis of a range of antibodies, and to define the distribution of axonal injury with flow and neurofilament markers in TAI. A further objective was to examine the expression of β-APP as an indicator of impaired axonal transport, three neurofilament markers targeting NF-160, NF-200, and the phosphorylated form of the neurofilament heavy chain (NFH), in different anatomical regions of piglet and human brains. The double immunofluorescence labelling method was then employed to investigate the hypothesis of co-localisation between β-APP and each one of the previous neurofilament markers. The animal studies showed significant differences in NF-160 between sham and injured 3-5 days old piglet cases (6 hour survival) and between 3-5 days sham and injured, when stained with SMI-34 antibody. In 4 weeks old piglet cases (6 hour survival), immunoreactivity of β-APP was significantly higher in injured than control. No other significant differences for any of the antibodies were noted, based on age, velocity, and survival time. Human results suggested that the brainstem had a higher level of β-APP and NF-160 than the corpus callosum and internal capsule. Co-localisation of β-APP with NFs was not a consistent feature of TAI in piglet and human brains, suggesting that markers of impaired axonal transport and neurofilament accumulation are sensitive to TAI, but may highlight different populations involved in the evolution of TAI.

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Malhotra, Rajiv. "GENE EXPRESSION FOLLOWING TRAUMATIC BRAIN INJURY." VCU Scholars Compass, 1998. http://scholarscompass.vcu.edu/etd/5082.

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The pathology which results from traumatic brain injury (TBI) have long been believed to be immediate and irreversible. However, recently it has been shown that, although the primary effects are virtually unavoidable, the secondary effects manifest themselves through biochemical processes set in motion at the time of the injury. These events are frequently mediated through the process of excitotoxicity, which results from a widespread release of excitatory neurotransmitters. These neurotransmitters go on to activate both ionotropic and metabotropic receptors. The signal transduction initiated through these receptor populations gives rise to changes in gene expression. One result of this release of neurotransmitter is an influx of calcium by means of excitatory receptors on the cell. The neurotransmitters upon which most research is focused are glutamate, aspartate, and acetylcholine. Current research is aimed at investigating antagonists to this process as well as elucidating steps within the process. Antagonists primarily function to reduce the calcium toxicity through modulation of receptor activity. However, the therapeutic window for effective antagonist usage is short. Therefore, although they may represent a viable treatment option, they need to be administered as early as possible following the injury to have the greatest effect. The purpose of this paper is to provide a summary of the available literature on TBI and excitotoxicity with a focus on changes in gene regulation. This paper will summarize information on the steps inVolved in the intracellular signaling cascade following brain injury and provide insight to further sites for regulation and treatment. This will also allow for development hypotheses on the possible roles of some of the genes whose expression is already known to be altered.

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Davies, Suzanne. "Personality change following traumatic brain injury." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397519.

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This thesis is submitted in partial fulfilment of the requirements for the degree of Clip. Psy, D. _ at the School of Psychology, University of Birmingham. It represents both the clinical work and research conducted over the course of the clinical training. Volume I contains the research components which are concerned with examining factors affecting adjustment following traumatic brain injury (TBI). The literature review explores-3 0 papers-written since 1998t hat examine the factors-purported to - affect the development of depression after a TBI. The empirical paper examines personality change following'TBI and includes the concurrent validation of a new measure of personality change in this population. Volume II contains five Clinical Practice Reports (CPRs) which were submitted over the course of the. clinical training. The first. four. reports represent the. core training components of the Clin. Psy. D. They include case examined from two psychological perspectives, a small-scale service-related report, a case study and a single-case experimental, design., The fifth report is a .case study from a. special t. paediatric neuropsychology placement. The fifth Clinical Practice Report was presented orally, therefore only-the abstract and references are presented.

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Macqueen, Ruth. "Masculine identity after traumatic brain injury." Thesis, University of East Anglia, 2016. https://ueaeprints.uea.ac.uk/60949/.

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Background: Men are twice as likely to experience a Traumatic Brain Injury (TBI) as women suggesting that aspects of masculine identity play an important role in how people acquire their brain injury. Research also suggests that masculine identity influences how people manage their health experiences. Masculine identity may therefore be an important consideration for neuropsychological therapy and rehabilitation more generally particularly because part of the process of rehabilitation concerns helping individuals with their sense of self. This research aimed to explore men’s experiences of masculine identity following TBI. Method: Individual interviews were conducted with 10 men age 21-67 who had experienced a TBI who were living in the community. Interpretative phenomenological analysis was used to consider lived experiences and to explore the meaning of the TBI experience in relation to masculine identity. Results: Three superordinate themes emerged from the analysis: Doing life and relationships differently: Participants identified changes in aspects of their role as a man within relationships, family, occupation and social groups. Self-perceptions and the perceived view of others: Self-perceptions and others perceptions of the ability to perform roles as a man resulted in experiences of shame and loss of self-confidence. The invisibility of the injury appeared to both accentuate and protect from the experience of shame. Managing the impact: Participants identified ways in which they thought about their lives and reformulated their behaviour in order to protect their identity as a man. Conclusions: The findings suggest that men experience changes in masculine identity following TBI, particularly when ideals about independence and roles were challenged. The findings highlight how masculine identity may be a valuable aspect of self in considering threats to and reconstruction of self-identity after TBI. Aspects of gender identity should be considered in order to promote engagement, support adjustment and achieve meaningful outcomes in rehabilitation.

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Helmy, Adel Ezzat. "Neuro-inflammation in traumatic brain injury." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610114.

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Books on the topic "Traumatic brain injury"

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Honeybul, Stephen, and Angelos G. Kolias, eds. Traumatic Brain Injury. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78075-3.

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Berwick, Donald, Katherine Bowman, and Chanel Matney, eds. Traumatic Brain Injury. Washington, D.C.: National Academies Press, 2022. http://dx.doi.org/10.17226/25394.

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Tsao, Jack W., ed. Traumatic Brain Injury. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-22436-3.

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Tsao, Jack W., ed. Traumatic Brain Injury. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-0-387-87887-4.

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Vos, Pieter E., and Ramon Diaz-Arrastia, eds. Traumatic Brain Injury. Chichester, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118656303.

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Greenwood, Richard. [Traumatic brain injury]. Nottingham: Headway National Head Injuries Association, 1991.

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Reitan, Ralph M. Traumatic brain injury. Tucson, Ariz: Neuropsychology Press, 1986.

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Gillard, Arthur. Traumatic brain injury. Detroit: Greenhaven Press, 2012.

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Cifu, David X. Traumatic brain injury. New York: Demos Medical Pub., 2010.

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W, Marion Donald, ed. Traumatic brain injury. New York: Thieme Medical, 1999.

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Book chapters on the topic "Traumatic brain injury"

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Traumatic Brain Injury." In Brain Metastases, 435–36. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_42.

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Wenthen, Richard, and Zoe A. Landers. "Traumatic Injury and Traumatic Brain Injury." In Essential Clinical Social Work Series, 215–39. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-31650-0_11.

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Athanasou, James A. "Traumatic Brain Injury." In Encountering Personal Injury, 117–29. Rotterdam: SensePublishers, 2016. http://dx.doi.org/10.1007/978-94-6300-657-6_11.

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Cioffi, William G., Michael D. Connolly, Charles A. Adams, Mechem C. Crawford, Aaron Richman, William H. Shoff, Catherine T. Shoff, et al. "Traumatic Brain Injury." In Encyclopedia of Intensive Care Medicine, 2297–311. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_871.

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Hayashi, Nariyuki, and Dalton W. Dietrich. "Traumatic Brain Injury." In Brain Hypothermia Treatment, 12–13. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53953-7_5.

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Agarwal, Vikas, and Samuel A. Tisherman. "Traumatic Brain Injury." In Imaging the ICU Patient, 365–75. London: Springer London, 2014. http://dx.doi.org/10.1007/978-0-85729-781-5_40.

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Vink, Robert, and Tracy K. McIntosh. "Traumatic Brain Injury." In Magnetic Resonance Spectroscopy and Imaging in Neurochemistry, 91–116. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5863-7_5.

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Tong, Karen, Barbara Holshouser, and Zhen Wu. "Traumatic Brain Injury." In Susceptibility Weighted Imaging in MRI, 171–90. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470905203.ch11.

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Hornstein, Andrew, and Glenn Seliger. "Traumatic Brain Injury." In Sexual and Reproductive Neurorehabilitation, 207–18. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2576-6_13.

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Zaninotto, Ana Luiza C., Beatriz Teixeira Costa, Isadora Santos Ferreira, Melanie French, Wellingson Silva Paiva, and Felipe Fregni. "Traumatic Brain Injury." In Neuromethods, 105–38. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7880-9_4.

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Conference papers on the topic "Traumatic brain injury"

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Ling, Geoffrey S. F., Jason Hawley, Jamie Grimes, Christian Macedonia, James Hancock, Michael Jaffee, Todd Dombroski, and James M. Ecklund. "Traumatic brain injury in modern war." In SPIE Defense, Security, and Sensing, edited by Šárka O. Southern. SPIE, 2013. http://dx.doi.org/10.1117/12.2020023.

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Fuchs, Franklin, Omar Kamal, Hanao Li, Mihye Ahn, and So Young Ryu. "Pediatric Patient Traumatic Brain Injury Prediction1." In 2020 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2020. http://dx.doi.org/10.1109/bibm49941.2020.9313568.

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Quang, Tri, Christopher Mela, Mingzhou Zhou, and Yang Liu. "Mobile traumatic brain injury assessment system." In 2018 IEEE International Symposium on Signal Processing and Information Technology (ISSPIT). IEEE, 2018. http://dx.doi.org/10.1109/isspit.2018.8705146.

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Gasimzade, G. Sh. "Early diagnosis of traumatic brain injury." In Global science. Development and novelty. НИЦ «Л-Журнал», 2019. http://dx.doi.org/10.18411/gdsn-25-12-2019-17.

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Zhang, Liying, King H. Yang, and Albert I. King. "A Proposed New Brain Injury Tolerance for Minor Traumatic Brain Injury." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/amd-25446.

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Abstract Traumatic brain injuries constitute a significant portion of injury resulting from automotive collisions, motorcycle crashes, and sports collisions. Brain injuries not only represent a serious trauma for those involved but also place an enormous burden on society, often exacting a heavy economical, social, and emotional price. Development of intervention strategies to prevent or minimize these injuries requires a complete understanding of injury mechanism, response and tolerance level. In this study, an attempt is made to delineate actual injury causation and establish a meaningful injury criterion through the use of the actual field accident data. Twenty-four actual field head-to-head collisions that occurred in professional football games were duplicated using a validated finite element human head model. The injury predictors and injury levels were analyzed based on resulting brain tissue responses and were correlated with the site and occurrence of MTBI. Prediction indicated that the shear deformation around the brainstem region could be an injury predictor for concussion. Statistical analyses were performed to establish the new brain injury tolerance level and to further reduce brain injury severity.

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Dolle, Jean-Pierre, Rene Schloss, and Martin L. Yarmush. "Simulating Diffuse Axonal Injury During Traumatic Brain Injury Events." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53414.

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Traumatic Brain Injuries (TBI) affect up to 1.5 million people annually within the United States with as many as 250,000 being hospitalized and 50,000 dying [1]. TBI events occur when the brain experiences a sudden trauma such as a rapid acc/deceleration. These events produce high inertial forces that result in a shearing or elongation of axons (commonly known as Diffuse Axonal Injury [2].

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Pillai, Nikhil, Abani Patra, and Ehsan Esfahani. "Modeling Post-Impact Injury Propagation in Traumatic Brain Injury." In ASME 2016 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/detc2016-60444.

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In this paper, we investigate the effect of mechanical deformation during original impact on the propagation of bleeds during traumatic brain injury (TBI). For this purpose, we have developed a numerical framework that considers Magnetic Resonance Images (MRI) of a rat subjected to TBI modelled using controlled cortical impact (CCI). Using the MRI images of first day of impact a solid model of brain is developed and strains during impact are estimated using the finite element tool LSDyna. It was observed that the actual propagation of blood obtained from day 14 MRI data closely resembles the one developed by solving a time dependent advection equation with advection rates proportional to the strain estimates during impact from LSDyna. This numerical framework holds promise that with proper calibration and validation it can be used to predict the possible propagation of blood post-impact and therefore may be used to inform treatment protocols for such patients.

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Shafiee, Abbas, Mohammad Taghi Ahmadian, and Maryam Hoviattalab. "Traumatic Brain Injury Caused by +Gz Acceleration." In ASME 2016 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/detc2016-59021.

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Traumatic brain injury (TBI) has long been known as one of the most anonymous reasons for death around the world. This phenomenon has been under study for many years and yet it remains a question due to physiological, geometrical and computational complexity. Although the modeling facilities for soft tissue have improved, the precise CT-imaging of human head has revealed novel details of the brain, skull and meninges. In this study a 3D human head including the brain, skull, and meninges is modeled using CT-scan and MRI data of a 30-year old human. This model is named “Sharif University of Technology Head Trauma Model (SUTHTM)”. By validating SUTHTM, the model is then used to study the effect of +Gz acceleration on the human brain. Damage threshold based on loss of consciousness in terms of acceleration and time duration is developed using Maximum Brain Pressure criteria. Results revealed that the Max. Brain Pressure ≥3.1 are representation of loss of consciousness. 3D domains for the loss of consciousness are based on Max. Brain Pressure is developed.

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Heller, Zachery E., Joseph Wyatt, and Jeffery C. Wolchok. "Development of a Traumatic Brain Injury Bioreactor." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14316.

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An in-vitro system was developed to mimic the impact deceleration and strain associated with concussive injuries. Similar in concept to a full scale crash test, the bench top concussive bioreactor can deliver decelerations from 0–250 g and biaxial strains from 5–25% to cells in culture. We are not aware of another system like this. From cellular testing, an injury threshold of 100g combined with 10% strain was identified. These values appear consistent with human brain injury data.

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Soroushmehr, S. M. R., A. Bafna, S. Schlosser, K. Ward, H. Derksen, and K. Najarian. "CT image segmentation in traumatic brain injury." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7319016.

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Reports on the topic "Traumatic brain injury"

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Dichter, Marc A. Preventing Epilepsy After Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada485727.

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Dichter, Marc A. Preventing Epilepsy After Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada452227.

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Dichter, Marc A. Preventing Epilepsy After Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada506626.

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Dichter, Marc A. Preventing Epilepsy after Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada468565.

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Mehegan, Laura. AARP Traumatic Brain Injury: Annotated Questionnaire. Washington, DC: AARP Research, October 2023. http://dx.doi.org/10.26419/res.00719.002.

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Najm, Imad. Deep Brain Stimulation of Treatment of Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada548984.

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DEPARTMENT OF DEFENSE WASHINGTON DC. Mild Traumatic Brain Injury Pocket Guide (CONUS). Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada529042.

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Walker, Mark. Disequilibrium after Traumatic Brain Injury: Vestibular Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada576379.

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Blakeman, Thomas C. Reducing Secondary Insults in Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada585415.

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Walker, Mark. Disequilibrium After Traumatic Brain Injury: Vestibular Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada559247.

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