Academic literature on the topic 'Major traumatic injury'

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Journal articles on the topic "Major traumatic injury"

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Cole, Elaine, Antonia Lynch, Jackie Bridges, and Anita West. "Older people and major trauma." Reviews in Clinical Gerontology 19, no. 2 (May 2009): 77–85. http://dx.doi.org/10.1017/s0959259809990177.

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SummaryMajor traumatic injury is a leading cause of death in younger age groups, but increasingly older people are affected also. Adverse outcomes, both physical and psychological, are associated with injury in the older population. This review aims to locate and describe the evidence relating to older people and major trauma in order to inform policy, practice, research and education. The published research and systematic reviews fall into three main topics: mechanism of traumatic injury in older people, the effects of co-morbidities on older trauma patients and outcomes following serious traumatic injury in older people. The psychological impact of traumatic injury and the resulting functional alteration cannot be underestimated in this group of patients.
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Herman, Carl D. "Major depression following traumatic brain injury." Journal of Head Trauma Rehabilitation 19, no. 4 (2004): 349. http://dx.doi.org/10.1097/00001199-200407000-00010.

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Jorge, Ricardo E., Robert G. Robinson, David Moser, Amane Tateno, Benedicto Crespo-Facorro, and Stephan Arndt. "Major Depression Following Traumatic Brain Injury." Archives of General Psychiatry 61, no. 1 (January 1, 2004): 42. http://dx.doi.org/10.1001/archpsyc.61.1.42.

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Finnie, J. W., and P. C. Blumbergs. "Traumatic Brain Injury." Veterinary Pathology 39, no. 6 (November 2002): 679–89. http://dx.doi.org/10.1354/vp.39-6-679.

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Animal models have played a critical role in elucidating the complex pathogenesis of traumatic brain injury, the major cause of death and disability in young adults in Western countries. This review discusses how different types of animal models are useful for the study of neuropathologic processes in traumatic, blunt, nonmissile head injury.
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Powelson, Elisabeth B., Brianna Mills, William Henderson-Drager, Millie Boyd, Monica S. Vavilala, and Michele Curatolo. "Predicting chronic pain after major traumatic injury." Scandinavian Journal of Pain 19, no. 3 (July 26, 2019): 453–64. http://dx.doi.org/10.1515/sjpain-2019-0040.

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Abstract Background and aims Chronic pain after traumatic injury and surgery is highly prevalent, and associated with substantial psychosocial co-morbidities and prolonged opioid use. It is currently unclear whether predicting chronic post-injury pain is possible. If so, it is unclear if predicting chronic post-injury pain requires a comprehensive set of variables or can be achieved only with data available from the electronic medical records. In this prospective study, we examined models to predict pain at the site of injury 3–6 months after hospital discharge among adult patients after major traumatic injury requiring surgery. Two models were developed: one with a comprehensive set of predictors and one based only on variables available in the electronic medical records. Methods We examined pre-injury and post-injury clinical variables, and clinical management of pain. Patients were interviewed to assess chronic pain, defined as the presence of pain at the site of injury. Prediction models were developed using forward stepwise regression, using follow-up surveys at 3–6 months. Potential predictors identified a priori were: age; sex; presence of pre-existing chronic pain; intensity of post-operative pain at 6 h; in-hospital opioid consumption; injury severity score (ISS); location of trauma, defined as body region; use of regional analgesia intra- and/or post-operatively; pre-trauma PROMIS Depression, Physical Function, and Anxiety scores; in-hospital Widespread Pain Index and Symptom Severity Score; and number of post-operative non-opioid medications. After the final model was developed, a reduced model, based only on variables available in the electronic medical record was run to understand the “value add” of variables taken from study-specific instruments. Results Of 173 patients who completed the baseline interview, 112 completed the follow-up within 3–6 months. The prevalence of chronic pain was 66%. Opioid use increased from 16% pre-injury to 28% at 3–6 months. The final model included six variables, from an initial set of 24 potential predictors. The apparent area under the ROC curve (AUROC) of 0.78 for predicting pain 3–6 months was optimism-corrected to 0.73. The reduced final model, using only data available from the electronic health records, included post-surgical pain score at 6 h, presence of a head injury, use of regional analgesia, and the number of post-operative non-opioid medications used for pain relief. This reduced model had an apparent AUROC of 0.76, optimism-corrected to 0.72. Conclusions Pain 3–6 months after trauma and surgery is highly prevalent and associated with an increase in opioid use. Chronic pain at the site of injury at 3–6 months after trauma and surgery may be predicted during hospitalization by using routinely collected clinical data. Implications If our model is validated in other populations, it would provide a tool that can be easily implemented by any provider with access to medical records. Patients at risk of developing chronic pain could be selected for studies on preventive strategies, thereby concentrating the interventions to patients who are most likely to transition to chronic pain.
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Taber, Katherine H., and Robin A. Hurley. "Traumatic Axonal Injury: Atlas of Major Pathways." Journal of Neuropsychiatry and Clinical Neurosciences 19, no. 2 (April 2007): iv—104. http://dx.doi.org/10.1176/jnp.2007.19.2.iv.

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Chambers, M. G., C. M. Airey, S. Chell, A. S. Rigby, J. Connelly, and A. Tennant. "A cost analysis of major traumatic injury." Injury 27, no. 5 (June 1996): 369. http://dx.doi.org/10.1016/0020-1383(96)86852-5.

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Thombs, Brett D. "Traumatic Brain Injury and Major Depressive Disorder." JAMA 304, no. 8 (August 25, 2010): 857. http://dx.doi.org/10.1001/jama.2010.1170.

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van Leeuwen, Nikki, Hester F. Lingsma, Pablo Perel, Fiona Lecky, Bob Roozenbeek, Juan Lu, Haleema Shakur, James Weir, Ewout W. Steyerberg, and Andrew I. R. Maas. "Prognostic Value of Major Extracranial Injury in Traumatic Brain Injury." Neurosurgery 70, no. 4 (April 2012): 811–18. http://dx.doi.org/10.1227/neu.0b013e318235d640.

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Khatri, Nidhi, Manisha Thakur, Vikas Pareek, Sandeep Kumar, Sunil Sharma, and Ashok Kumar Datusalia. "Oxidative Stress: Major Threat in Traumatic Brain Injury." CNS & Neurological Disorders - Drug Targets 17, no. 9 (November 2, 2018): 689–95. http://dx.doi.org/10.2174/1871527317666180627120501.

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Background & Objective: Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion: In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.
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Dissertations / Theses on the topic "Major traumatic injury"

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Connelly, James Bernard. "Outcome of major traumatic injury." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413207.

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Books on the topic "Major traumatic injury"

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Hart, Tessa. Cognitive Enhancement in Traumatic Brain Injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190214401.003.0006.

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Traumatic brain injury (TBI) is a prevalent source of disability. This chapter reviews the major approaches to remediation of cognitive dysfunction following TBI, in both the early and post-acute phases of recovery. Pharmacologic and behavioral treatments are discussed, focusing on the three major areas of cognition affected by TBI: attention, memory, and executive function. Trials of pharmacologic treatments, especially neuroprotective agents, have resulted in few treatment guidelines, probably due to the heterogeneous pathophysiology of TBI. Among behavioral treatments, both restorative and compensatory approaches are presented. Most of the available evidence favors compensatory treatments, in which patients are taught alternative strategies and/or changes are made in the social/physical environments to facilitate everyday functioning. Despite methodologic challenges and limitations in treatment definition that make comparisons across studies difficult, cognitive rehabilitation for TBI is increasingly viewed as a vital component of the effort to restore maximal independence at home and in society.
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Aisiku, Imoigele, and Claudia S. Robertson. Epidemiology and pathophysiology of traumatic brain injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0341.

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Although medical management of traumatic brain injury (TBI) may have improved in developed countries, TBI is still a major cause of mortality and morbidity. The demographics are skewed towards the younger patient population, and affects males more than females, but in general follow a bimodal distribution with peaks affecting young adults and the elderly. As a result, the loss of functional years is devastating. Pathology due to brain trauma is a complex two-hit phenomenon, frequently divided into ‘primary’ and ‘secondary’ injury. Hypoxia, ischaemia, and inflammation all play a role, and the importance of each component varies between patients and in an individual patient over time. The initial injury may increase intracranial pressure and reduce cerebral perfusion due to the presence of mass lesions or diffuse brain swelling. Further secondary insults, such as hypotension, reduced cerebral perfusion pressure, hypoxia, or fever may exacerbate swelling and inflammation, and further compromise cerebral perfusion. Although there are currently no specific effective treatments for TBI, an improved understanding of the pathophysiology may eventually lead to treatments that will reduce mortality and improve long-term functional outcome.
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Varley, Patrick R., and Louis H. Alarcon. Major Trauma (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0012.

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Trauma is a leading cause of death and disability in the United States. Although it is generally considered to occur mostly outside of the hospital, traumatic injuries may occur anywhere. Outcomes for patients experiencing major trauma are closely linked to the healthcare response. Appropriate responses to traumatic injuries have been developed over the past 50 years, and are now considered to involve the care of a well-trained trauma team. This team utilizes established protocols to rapidly evaluate and treat injured patients. This chapter discusses the evolution of trauma teams, equipment and supplies, and the primary, secondary, and tertiary surveys used in trauma team response.
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Beheiry, Hossam El. Neurophysiology/Neuroprotection. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0027.

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Intracerebral hemorrhage (ICH) is a catastrophic event that may lead to severe disability or death. It is associated with major disruption of intracranial neurophysiology and subsequent neuronal tissue injury. The etiology of ICH may be primary (e.g., hypertensive) or secondary (e.g., traumatic). Treatment options include conservative management or neurosurgical intervention in selected patients. In order to manage these challenging cases, the anesthesiologist and the intensivist should have thorough knowledge pertaining to neurophysiologic concepts of cerebral blood flow, cerebral autoregulation, and neuroprotection principles. Additionally, the specialized team managing the patient with ICH should be cognizant of the most recent evidence-based guidelines recommended by the pertinent associations.
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Wong, Victoria S. S., and Martin Salinsky. Neurological and Medical Factors. Edited by Barbara A. Dworetzky and Gaston C. Baslet. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190265045.003.0004.

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This chapter addresses the neurological and medical factors associated with psychogenic nonepileptic seizures (PNES). PNES can occur concurrently with epilepsy in 5 to 20% of patients. Traumatic brain injury (TBI) is a major cause of epilepsy, but it is also commonly cited by patients with PNES as the primary cause of their seizures. PNES are also overrepresented in patients with intellectual and learning disabilities. Patients with PNES usually have additional subjective neurological and medical complaints. Pain complaints are overrepresented in patients with PNES and are a major contributor to health care use. Cognitive complaints are also common, with a patient’s mood playing a larger role than objective cognitive dysfunction. Medically unexplained symptoms such as fibromyalgia and chronic fatigue syndrome are overrepresented in patients with PNES. Their occurrence increases the likelihood of diagnosing PNES over epilepsy. These observations reveal a complex pattern of susceptibility to the development of PNES. PNES are thus best viewed as only one symptom of a heterogeneous disorder characterized by multiple physical symptoms used to express psychological distress.
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Gray, Francoise, Charles Duyckaerts, and Umberto de Girolami, eds. Escourolle and Poirier's Manual of Basic Neuropathology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190675011.001.0001.

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Escourolle and Poirier’s Manual of Basic Neuropathology is a monograph on neuropathology that provides classic macroscopic and microscopic descriptions of the pathology of diseases of the nervous system complemented with the most up-to-date accounts of the pathophysiology, genetics, and molecular biology of these diseases. The book is divided into 14 chapters that cover all the major categories of neurological diseases. The chapter topics are as follows: 1, introduction to the basic reactions of the nervous system; 2, neoplasms; 3, traumatic injury; 4, vascular disease; 5, infectious disease; 6, prion disease; 7, demyelinating disease; 8, degenerative disease; 9, acquired metabolic disease; 10, hereditary metabolic disease; 11, congenital malformations and perinatal disease; 12, disease of skeletal muscle; 13, disease of peripheral nerve; and 14, disease of the pituitary gland. An Appendix gives an overview of the technical aspects of laboratory study of the nervous system, including the latest concepts in molecular diagnosis.
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Book chapters on the topic "Major traumatic injury"

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Hazeldine, Jon, and Mark Foster. "The Immune and Inflammatory Response to Major Traumatic Injury." In Blast Injury Science and Engineering, 147–60. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-10355-1_13.

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Shetye, Omkar Anand. "Dentoalveolar Injuries and Wiring Techniques." In Oral and Maxillofacial Surgery for the Clinician, 1013–37. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-1346-6_50.

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AbstractTraumatic dental injuries account for majority of maxillofacial injuries affecting soft tissues as well as maxillofacial bones. History of immediate local measures employed to reduce the severity of injury helps in eliciting information regarding the original condition of the injured area. Time elapsed post trauma plays a major role in determining outcome of the intervention. Goal of the treatment is directed towards achieving the pre-traumatic occlusion and intra arch contour.
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Hategan, Ana, James A. Bourgeois, Tracy Cheng, and Julie Young. "Other Major and Mild Neurocognitive Disorders: Parkinson Disease, Atypical Parkinsonism, and Traumatic Brain Injury Types." In Geriatric Psychiatry Study Guide, 243–68. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77128-1_10.

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Cross, F. W. "Major acute traumatic injury." In Hutchison's Clinical Methods, 425–39. Elsevier, 2007. http://dx.doi.org/10.1016/b978-0-7020-2799-4.50027-3.

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Rao, Vani. "Traumatic Brain Injury." In Psychiatric Aspects of Neurologic Diseases. Oxford University Press, 2008. http://dx.doi.org/10.1093/oso/9780195309430.003.0011.

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Traumatic brain injury (TBI) is a significant cause of disability in the United States, with an incidence of about 1.5 million cases per year (National Institutes of Health Consensus Development Panel, 1999). It is associated with both neurologic and psychiatric consequences. Although the neurologic problems usually stabilize with time, the psychiatric disorders often continue to remit and relapse. Factors associated with the development of psychiatric disorders include older age, arteriosclerosis, and chronic alcoholism, all of which interfere with the reparative process within the central nervous system. Other contributors to psychiatric disability include a pre-TBI history of psychiatric illness, illicit drug abuse, and lack of social support. Because post-TBI psychiatric disturbances interfere with rehabilitation and cause emotional and financial burden for patients and caregivers, early diagnosis and treatment are important. Post-TBI psychiatric disturbances are best classified according to their clinical presentation. These disturbances are discussed below and their pharmacologic and nonpharmacologic treatment strategies are recommended. The mood disturbances most commonly associated with TBI are major depression, mania, anxiety, and apathy. Major depression is seen in about 25% of people with TBI. Symptoms of major depression include persistent sadness; guilt; feelings of worthlessness; hopelessness; suicidal thoughts; anhedonia; and changes in patterns of sleep, appetite, and energy. Sometimes these symptoms may be associated with psychotic features such as delusions and hallucinations. It is important to remember that changes in sleep, appetite, or energy are not specific to the syndrome of major depression and may be due to the brain injury itself, or to the noise, stimulation, or deconditioning associated with hospitalization. If due to the latter conditions, gradual improvement occurs with time in most patients. Sadness in excess of the severity of injury and poor participation in rehabilitation are strong indicators of the presence of major depression. The presence of poor social functioning pre-TBI and left dorsolateral frontal and/or left basal ganglia lesion have been associated with an increased probability of developing major depression following brain injury ( Jorge et al., 1993a; Jorge et al., 2004). Major depression should be differentiated from demoralization, primary apathy syndrome, and pathologic crying.
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Wyatt, Jonathan P., Robert G. Taylor, Kerstin de Wit, Emily J. Hotton, Robin J. Illingworth, and Colin E. Robertson. "Major trauma." In Oxford Handbook of Emergency Medicine, 328–407. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198784197.003.0008.

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This chapter in the Oxford Handbook of Emergency Medicine investigates major trauma in the emergency department (ED). It reviews general treatment principles, resuscitation, and investigations, and explores airway obstruction, tension pneumothorax, rib fractures, sternal fracture, flail segment, ruptured diaphragm, oesophageal rupture, traumatic pneumothorax, haemothorax, chest drain insertion, pulmonary contusions and aspiration, penetrating chest injury, open chest injury, traumatic cardiac arrest, thoracotomy for cardiac arrest, aortic injury, focused assessment with sonography for trauma (FAST) scan, blunt abdominal trauma, penetrating abdominal trauma, renal trauma, bladder injury, urethral trauma, scrotal and testicular trauma, minor and serious head injury, post-concussion symptoms, carotid/vertebral artery dissection, maxillofacial injuries, mandibular injuries, temporomandibular joint dislocation, penetrating neck trauma, silver trauma, spine and spinal cord injury, dermatomes, gunshot injuries, blast injuries, burns, inhalation injury, and crush syndrome.
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Dodd, Oliver, Alex Wickham, Oliver Dodd, Alex Wickham, Oliver Dodd, Alex Wickham, Edwin Clitheroe, Fleur Cantle, and Nicholas Freeman. "The major trauma patient." In Oxford Handbook of Anaesthesia, 967–1032. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198853053.003.0037.

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This chapter describes the anaesthetic management of the major trauma patient. It begins with immediate trauma care, the patient journey, primary survey and resuscitation. The management of head and traumatic brain injury, thoracic injury, abdominal and pelvic injuries, spinal injury, limb and extremity injury, blast injury and gunshot wounds and traumatic cardiac arrest are discussed. The specific management of burns, paediatric trauma and silver trauma are covered. Anaesthesia for major trauma, including damage control resuscitation and damage control surgery are discussed.
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Wyatt, Jonathan P., Robin N. Illingworth, Colin A. Graham, Kerstin Hogg, Michael J. Clancy, and Colin E. Robertson. "Major trauma." In Oxford Handbook of Emergency Medicine, 319–400. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199589562.003.0008.

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Major trauma: treatment principles 320 Investigations in major trauma 322 Airway obstruction: basic measures 324 Airway obstruction: surgical airway 326 Tension pneumothorax 328 Chest wall injury 330 Traumatic pneumothorax 334 Haemothorax 335 Chest drain insertion 336 Pulmonary contusions and aspiration 338 Penetrating chest injury 340...
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Johansson, Birgitta, and Lars Rnnbck. "Long-Lasting Mental Fatigue After Traumatic Brain Injury – A Major Problem Most Often Neglected Diagnostic Criteria, Assessment, Relation to Emotional and Cognitive Problems, Cellular Background, and Aspects on Treatment." In Traumatic Brain Injury. InTech, 2014. http://dx.doi.org/10.5772/57311.

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Coetzer, Rudi. "Major depressive disorder." In Anxiety and Mood Disorders Following Traumatic Brain Injury, 157–75. Routledge, 2018. http://dx.doi.org/10.4324/9780429471841-10.

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Conference papers on the topic "Major traumatic injury"

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Falcão, Rafael Tenório, Alexandre Gabriel Taumaturgo Cavalcanti Arruda, Wagner Gonçalves Horta, Douglas de Albuquerque Veiga Vieira, and Guilherme de Souza Silva. "Rehabilitation in traumatic brain injury due to automobile accident." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.032.

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Background: Automobile accidents (AA) stand as public health issue, being the second most prevalent cause of preventable unnatural death in Brazil. Traumatic brain injury (TBI) has a strong relationship with AA, with a high incidence of morbidity and mortality. Due to the wide spectrum of possible sequel, rehabilitation is essential to help patients to restore functionality and improve quality of life. Objectives: We sought to evaluate and characterize rehabilitation in cases of TBI, resulting from AA. Design and setting: This is an integrative literature review carried out by medical students from the University of Pernambuco. Methods: The databases BVS, PubMed and SciELO were used in this research together with the following descriptors: “Prognosis”, “Accidents, Traffic”, “Brain Injuries, Traumatic” and “Rehabilitation”. The focus was on articles published in Portuguese, Spanish and English between the years 2011 and 2021. Among the 44 articles found, only 06 were suitable to the research. Results: When compared the results of rehabilitation in specialized unit and those in non-specialized unit there were notable difference. Despite the longer hospital stay, the specialized units allowed for better recovery and greater functional independence for their patients. It was made clear that, even in cases of mild TBI, rehabilitation minimized functional impairments and improved recovering patient’s quality of life. Conclusions: It is necessary to expand the specialized units for better rehabilitation of patients with TBI, due to the treatment place being a major component in the process. The specialized units demonstrated considerable efficiency when compared to the non-specialized units.
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Li, Jianrong, Jiangyue Zhang, Narayan Yoganandan, Frank A. Pintar, and Thomas A. Gennarelli. "Rotational Acceleration Duration Affects Brain Strains in Lateral Impact." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176358.

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Traumatic brain injury is a leading cause of disability and fatality in the United States. Approximately two million traumatic brain injury cases occur every year [1]. Motor vehicle crashes are a primary source [2]. Both clinical and laboratory studies have been conducted to understand injury mechanisms and establish injury thresholds [3, 4]. Physical models have also been used to investigate injury biomechanics [5, 6]. Angular acceleration is considered as a major cause of diffuse brain injuries (DBI) [7, 8], while the angular velocity is chosen as a suitable load descriptor for a diffuse brain injury criterion [4]. The present study is focused on the effect of angular acceleration duration on brain strains due to lateral impact.
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Laksari, Kaveh, Mobin Rastgar Agah, and Kurosh Darvish. "Hyperelastic Behavior of Porcine Aorta in Sub-Injury Pressures." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80871.

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Traumatic Aortic Rupture (TAR) is a major cause of fatality in motor vehicle crashes. In terms of numbers, only 9% of the subjects who experience such trauma (7500–8000 victims in US and Canada) survive from the scene of the accident and the overall mortality rate is 98% [1].
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Przekwas, Andrzej, V. C. Chancey, X. G. Tan, Z. J. Chen, P. Wilkerson, A. Zhou, V. Harrand, C. Imielinska, and D. Reeves. "Development of Physics-Based Model and Experimental Validation of Helmet Performance in Blast Wave TBI." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206839.

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Explosive devices are the main weapon of terrorist attacks and a cause of major injuries to Soldiers and civilians. Recent military medical statistics show that a significant percentage of Soldiers injured in explosion events endures blast wave traumatic brain injury (BW-TBI). In the last few years, better understandings of BW-TBI mechanisms and of improved injury protection have become of paramount importance. Most studies have taken the conventional approach of animal testing, in vitro brain tissue study, and analysis of clinical data. These, while useful and necessary, are slow, expensive, and often non-conclusive. Physiology-based mathematical modeling tools of blast wave brain injury will provide a complementary capability to study both BW-TBI mechanisms and the effectiveness of protective armor.
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Abrantes, Maely Moreira de. "Predictive factors in the prognosis of victims of trauma crisis in brain." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.315.

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Background: Among mechanical traumas, traumatic brain injury (TBI) is the main determinant of deaths and sequelae in polytrauma patients. TBI is defined as any traumatic injury to the brain that results in anatomical injury such as skull fracture or scalp injury, functional impairment of the meninges, brain and its vessels or momentary or permanent brain changes, of a cognitive or physical nature. Objective: The present work aims to conduct a literature review on the factors that are predictive in the prognosis of victims of traumatic brain injury. Methods: This is a literature review based on the medical literature and scientific articles indexed in the Scientific Eletronic Library Online (SCIELO) and VHL-Brazil. Results: Several factors are related to a worse prognosis in patients suffering from TBI, and the most cited are: score equal to or less than 8 on the Glasgow Coma Scale (ECG) on admission; age over 60 years; tomographic changes showing diffuse axonal lesion or cerebral edema; pupils with abolished photomotor reflexes; arterial hypotension at admission; hyperthermia and male sex. Studies address that the initial clinical-neurological severity, measured by ECG, has the greatest significant influence on the evolution of patients, showing that the initial clinical manifestation points out the severity of primary and secondary injuries associated with TBI. As well as ECG, several other factors such as the brain’s susceptibility to injury, the extent and severity of the injuries, the presence of global or focal injuries, associated injuries and the initial response to treatment are also cited as useful in determining the evolution of cases of victims of TCE. Conclusions: It was found that the TBI is the main responsible for high lethality rates in polytrauma patients worldwide and from obtaining these data in recent years, studies have been deepened in order to search for the prognostic factors for TBI. The identification of these indicators has represented a major advance in the search for alternatives to guide the treatment of the patient and estimate the final result.
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Tan, X. Gary, Andrzej J. Przekwas, and Raj K. Gupta. "Macro-Micro Biomechanics Finite Element Modeling of Brain Injury Under Concussive Loadings." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-66218.

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Traumatic brain injury (TBI) occurs in many blunt, ballistic and blast impact events. During trauma axons in the white matter are especially vulnerable to injury due to the rapid mechanical loading of brain. The axonal pathology leads to cytoskeletal failure and disconnection. The microtubules are one of major structural components of the cytoskeleton filamentous network. By bridging the macroscopic forces acting on the whole brain with the cellular and subcellular failure, the macro-micro computational models in both time and space can help us better understand the complex biophysics and elucidate the injury mechanism of both severe and mild TBI (concussion). At the macroscopic scale we developed the high-fidelity anatomical human body finite element model (FEM) to predict intracranial pressures and strain and strain rate fields of brain in the blast event. The macro-scale models and the coupled blast and biomechanics approach were validated against test data of shock wave interacting with a surrogate head in the shock tube. The mechanical deformation of brain tissue was mapped to the white matter tracts to obtain local axonal strain and strain rate for the micromechanical models. We developed the micromechanical FEM of myelinated axons interconnected with the oligodendrocyte by the processes, utilizing a novel beam element free of rotational degrees of freedom (DOFs). The numerical results reveal the possible mechanism of impact-induced axon injury including demyelination, breakup of processes, and axonal varicosity. We also investigate the dynamic response of microtubules bundles under traumatic loading. Different from the commonly discrete bead-spring models, a network of microtubules cross-linked with microtubule-associated-protein (MAP) tau proteins was modeled by the nonlinear beam model. Tau protein is modeled by the rate-dependent bar element for its complicated material behavior. The model considers the rupture of microtubule and the failure of tau-tau interface and tau-microtubule interface. The simulation result of the combined effects of the failure of the cross-linked architecture and elongation and bending of the bundle are possibly correlated to the axonal undulations following traumatic loading observed in the experiments. The developed macro-micro biomechanics models can be used as a starting point for modeling the neurobiology effects and guide the design of novel injury protection strategies.
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7

Ott, Kyle, Liming Voo, Andrew Merkle, Alexander Iwaskiw, Alexis Wickwire, Brock Wester, and Robert Armiger. "Experimental Determination of Pressure Wave Transmission to the Brain During Head-Neck Blast Tests." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14834.

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Traumatic Brain Injury (TBI) has been the termed the “signature injury” in wounded soldiers in recent military operations [1]. Evidence has shown a strong association between TBI and blast loading to the head due to exposure to explosive events [2, 3]. Head injury mechanisms in a primary blast environment remain elusive and are the subject of much speculation and hypotheses. However, brain injury mechanisms have traditionally been attributed to either a direct impact or a rapid head acceleration or deceleration. Extensive research has been performed regarding the effects of blunt trauma and inertial loading on head injuries [4, 5]. Direct impacts to the head can largely be described based on linear acceleration measurements that correlate to skull fracture and focal brain injuries [6]. Computational head modeling of blunt impact events has shown that the linear acceleration response correlates well with increases in brain pressure [7]. Intracranial pressure, therefore, has been one of the major quantities investigated for correlation to blast induced TBI injury mechanisms [8–14].
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8

Assari, Soroush, Kaveh Laksari, Mary Barbe, and Kurosh Darvish. "Cerebral Blood Pressure Rise During Blast Exposure in a Rat Model of Blast-Induced Traumatic Brain Injury." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-64992.

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Blast-induced traumatic brain injury (bTBI) has been called the signature wound of war in the past decade. The mechanisms of such injuries are not yet completely understood. One of the proposed hypotheses is the transfer of pressure wave from large torso blood vessels to the cerebrovasculature as a major contributing factor to bTBI. The aim of this study was to investigate this hypothesis by measuring cerebral blood pressure rise during blast exposure and comparing two scenarios of head-only or chest-only exposures to the blast wave. The results showed that the cerebral blood pressure rise was significantly higher in chest-only exposure, and caused infiltration of blood-borne macrophages into the brain. It is concluded that a significantly high pressure wave transfers from torso to cerebrovasculature during exposure of the chest to a blast wave. This wave may lead to blood-brain barrier disruption and consequently trigger secondary neuronal damage.
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9

Hoursan, Hesam, Mohammad Taghi Ahmadian, Ahmad Barari, and Hamid Naghibi Beidokhti. "Modelling and Analysis of the Effect of Angular Velocity and Acceleration on Brain Strain Field in Traumatic Brain Injury." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-63053.

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Traumatic brain injury (TBI) has long been known as one of the most anonymous reasons for death around the world. A presentation of a model of what happens in the process has been under study for many years; and yet it remains a question due to physiological, geometrical and computational complications. Although the facilities for soft tissue modeling have improved and the precise CT-imaging of human head has revealed novel details of brain, skull and the interface (the meninges), a comprehensive FEM model of TBI is still being studied. This study aims to present an optimized model of human head including the brain, skull, and the meninges after a comprehensive study of the previous models. The model is then used to investigate the effects of various sudden velocity-acceleration impulses on the strain field of the brain by using FE method. Next, the results are summed up and compared with an existing criterion on damage threshold in the brain during trauma. To reach this aim, a full geometrical model of a 30-year-old patient’s head has been generated from CT-scan and MR data. The model has been exposed to 20 angular velocity-acceleration pulses. Subsequently, the changes in the strain field have been compared with the results obtained in the previous studies yielding acceptable accordance with a major previous criterion. The results also show that certain criteria can be generated on the threshold of damage in the brain.
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10

Wang, Chenzhi, Jae Bum Pahk, Carey D. Balaban, Joseph Muthu, David A. Vorp, Mark C. Miller, and Jeffrey S. Vipperman. "Biomechanical Assessment of the Bridging Vein Rupture of Blast-Induced Traumatic Brain Injury Using the Finite Element Human Head Model." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-88739.

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The incidence of the blast-induced traumatic brain injury (bTBI) among American troops in battle environments is dramatically high in recent years. Shock wave, a production of detonation, is a brief and acute overpressure wave that travels supersonically with a magnitude which can be several times higher than atmospheric pressure. Primary bTBI means that human exposure to shock wave itself without any other impact of solid objects can still result in the impairment of cerebral tissues. The mechanism of this type of brain injury is different from that of the conventional TBI, and has not been fully understood. So far, it is believed that the shock wave transmitted through skull and into cerebral tissues may induce specific injury patterns. This study is trying to develop a methodology to numerically investigate the mechanism of the blast-induced subdural hematoma (bSDH), which is caused by bridging vein rupture. The effort of this study can be divided to three major parts: first, a finite element (FE) model of human head is developed from the magnetic resonance imaging (MRI) of a real human head to contain skull, CSF and brain. Numerically simulated shock waves transmits through the human head model whose mechanical responses are recorded; second, in order to obtain the mechanical properties of human bridging vein, an standard inflation test of blood vessels is conducted on a real human bridging vein sample gained from autopsy. Material parameters are found by fitting the experimental data to an anisotropic hyperelastic constitutive model for blood vessel (Gerhard A. Holzapfel 2000); third, The bridging vein rupture in bTBI is evaluated by the finite element analysis of a separate human bridging vein model under the external loadings in terms of the internal pressure and relative skull-brain motion which are extracted from the mechanical response of the subarachnoid space of the head in the blast-head simulation of the first part.
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