Primary brain injury, due to initial injury forces, causes tissue distortion and destruction in the early postinjury period. Clinical outcomes depend in large part on mediating the bimolecular and cellular changes that occur after the initial injury. These secondary injuries from traumatic brain injury lead to alterations in cell function and propagation of injury through processes such as depolarization, excitotoxicity, disruption of calcium homeostasis, free‐radical generation. IntroductionIndividuals of all ages, background, and health status are susceptible to traumatic brain injury (TBI). Every year in the United States 1.7 million people suffer TBI and TBI is listed as a contributing cause in approximately one third of injury-related deaths . While the numbers suggest a grim state concerning TBI treatment there have been improvements in its management. Over the past 30 years, deaths from severe TBI have reduced from 50% to fewer than 25% . Evidence-based. Traumatic brain injury: pathophysiology for neurocritical care Kosaku Kinoshita Abstract Severe cases of traumatic brain injury (TBI) require neurocritical care, the goal being to stabilize hemodynamics and systemic oxygenation to prevent secondary brain injury. It is reported that approximately 45 % of dysoxygenatio .. The pathophysiology of traumatic brain injury at a glance. 9 Pages. The pathophysiology of traumatic brain injury at a glance . Disease Models & Mechanisms, 2013. Mayumi Prins. Christopher Giza. Mayumi Prins. Christopher Giza. Download PDF. Download Full PDF Package. This paper. A short summary of this paper. 37 Full PDFs related to this paper. READ PAPER.
Traumatic brain injury pathophysiology pdf brain injury by an external source traumatic brain injury other intracranial names, brain injury induced physically tic scanning showing brain contusions, hemorrhage within hemispheres, subduration hematoma, and fractures of the skullSpecialtyNeurosurgery, pediatricsmptomsphysical, cognitive, sensory, social, emotional an Traumatic brain injury (TBI) is defined as an impact, penetration or rapid movement of the brain within the skull that results in altered mental state. TBI occurs more than any other disease, including breast cancer, AIDS, Parkinson's disease and multiple sclerosis, and affects all age groups and both genders. In the US and Europe, the magnitude of this epidemic has drawn national attention owing to the publicity received by injured athletes and military personnel. This.
Traumatic brain injury (TBI) has become the signature injury of the military conflict in Iraq and Afghanistan and also has a high rate of occurrence in civilian populations in the United States. Although the effects of a moderate to severe brain injury have been investigated for decades, the chronic effects of single and repetitive mild TBI are just beginning to be investigated. Data suggest that the different types and severities of TBI have unique long-term outcomes and thus may represent. Schematic representation of pathophysiology of traumatic brain injury (TBI). BBB dysfunction caused by TBI insult allows transmigration of activated leukocytes into the injured brain parenchyma, which is facilitated by an upregulation of cell adhesion molecules. Activated leukocytes, microglia and astrocytes produce ROS and inflammatory molecules such as cytokines and chemokines that contribute to demyelination and disruption of axonal cytoskeleton, leading to axonal swelling and.
Traumatic brain injury pathophysiology features persistent depolarization of neuronal cells and astrocytes. This leads to the over-stimulation of ionotropic and metabotropic glutamate receptors with consecutive sodium, potassium, and calcium fluxes. To restore normal ionic gradients, the brain demands production of energy for restoring ionic homeostasis. But because of inadequate cerebral. Traumatic brain injury is a major source of death and disability worldwide. Significant success has been achieved in improving short-term outcomes in severe traumatic brain injury victims; however, there are still great limitations in our ability to return severe traumatic brain injury victims to high levels of functioning Traumatic brain injury (TBI) is an insult to the brain from an external mechanical force. It may cause permanent or temporary impairment of cognitive, physical, and/or psychological functions. It may also be associated with an altered or diminished state of consciousness. It accounts for approximately 40% of all deaths from acute injuries. The economic burden due to loss of earning capacity is.
. TBI is frequently referred to as the silent epidemic because the complications from TBI, such as changes affecting thinking, sensation, language, or emotions, may not be readily apparent. In addition, awareness about TBI among the general public is limited. Through the TBI Act of 1996 (Public Law 104. General pathophysiology of traumatic brain injury. The first stages of cerebral injury after TBI are characterized by direct tissue damage and impaired regulation of CBF and metabolism. This 'ischaemia-like' pattern leads to accumulation of lactic acid due to anaerobic glycolysis, increased membrane permeability, and consecutive oedema formation. Since the anaerobic metabolism is inadequate to maintain cellular energy states, the ATP-stores deplete and failure of energy.
Traumatic brain injury (TBI) constitutes the primary reason for mortality and morbidity in persons worldwide below 45 years of age. 1.7 million Traumatic events occur yearly in the United States alone, considering for 50,000 deaths. In severe traumatic brain injury sufferers, a considerable achievement attained in treating short-term conse-quences; but till date, huge failures are occurring in. Clinical outcomes depend in large part on mediating the bimolecular and cellular changes that occur after the initial injury. These secondary injuries from traumatic brain injury lead to alterations in cell function and propagation of injury through processes such as depolarization, excitotoxicity, disruption of calcium homeostasis, free-radical generation, blood-brain barrier disruption, ischemic injury, edema formation, and intracranial hypertension. The best hope for improving. Pathophysiology of Secondary Cerebral Damage after Traumatic Brain Injury. A schematic view of the pathophysiology of secondary cerebral damage after traumatic brain injury that supports the concept of optimizing cerebral blood flow, the delivery of oxygen and the adequate supply of energy substrates
Traumatic brain injury (TBI) is one of the leading causes of death of young people in the developed world. In the United States alone, 1.7 million traumatic events occur annually accounting for 50,000 deaths. The etiology of TBI includes traffic accidents, falls, gunshot wounds, sports, and combat-related events. TBI severity ranges from mild to severe. TBI can induce subtle changes in molecular signaling, alterations in cellular structure and function, and/or primary tissue. Referred to as a silent epidemic, traumatic brain injury (TBI) is a leading cause of death and disability among children and young adults, with millions of people sustaining TBI each year in accidents, sports, and military conflicts (1-3). TBI may lead to potentially long-lasting neurological dysfunctions, memory disturbances, behavioral changes, speech irregularities, and gait abnormalities. It has also been implicated in the development of neurodegenerative disease. Pathophysiology of Traumatic Brain Injury Melissa J. McGinn, PhD, John T. Povlishock, PhD* Traumatic brain injury (TBI) remains one of the most complex diseases known in the most com-plex of all organs in the body. The causes of TBI are many and varied and include penetrating and nonpenetrating injuries that, based on their overall level of severity, can evoke different degrees of morbidity. Pathophysiology of traumatic brain injury Andrew Sas M.D. Ph.D. Ohio State University Medical Center Department of Neurology OSU CBI Neuro‐Nights 07/09/2020. Disclosures • Neurologist and physician scientist at Ohio State Medical Center • I split my time between clinical care of patients with traumatic brain injuries (TBI) and research in a lab and clinic exploring the immune response to.
Objective - To review current information regarding the pathophysiology associated with traumatic brain injury (TBI), and to outline appropriate patient assessment, diagnostic, and therapeutic options. Etiology - TBI in veterinary patients can occur subsequent to trauma induced by motor vehicle accidents, falls, and crush injuries Pathophysiology of Traumatic Brain Injury Neurosurg Clin N Am. 2016 Oct;27(4):397-407. doi: 10.1016/j.nec.2016.06.002. Epub 2016 Aug 10. Authors Melissa J McGinn 1 , John T Povlishock 2 Affiliations 1 Department of Anatomy and Neurobiology, Medical College of. Traumatic brain injury: pathophysiology and emergency management K. Hoppe1 · W. Klingler2 Schädel-Hirn-Trauma: Pathophysiologie und Notfallmanagement Zitierweise: Hoppe K, Klingler W: Schädel-Hirn-Trauma: Pathophysiologie und Notfallmanagement. Anästh Intensivmed 2021;62:118-127. DOI: 10.19224/ai2021.118 Zusammenfassung Das Schädel-Hirn-Trauma (SHT) stellt den häufigsten Grund für.
In patients with traumatic brain injury (TBI), AMS can be defined as neurological deterioration relative to their baseline level of consciousness 2. The common causes of AMS in TBI patients occur in the following categories: TRIUMPH Tele-Rehabilitation Interventions through University-based Medicine for Prevention and Health TRAUMATIC BRAIN INJURY GUIDELINES 2020 TRIUMPH TRAUMATIC BRAIN INJURY. . It is reported that approximately 45 % of dysoxygenation episodes during critical care have both extracranial and intracranial causes, such as intracranial hypertension and brain edema Pathophysiology of traumatic brain injury By Amir Rezagholizadeh 2. Reference 2 3. Outline • Introduction • Etiology • Classification • Symptoms • General pathophysiology of TBI • Specific pathophysiology of TBI • References 3 4. Introduction • Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. TBITBI PDPD.
Abstract. Traumatic brain injury continues to increase in incidence and is associated with severe disability and limited treatment options. Neurotrauma research seeks to preserve, support and augment the recovery of the central nervous system from the effects of secondary brain injury, the sequelae of the initial impact Traumatic brain injury (TBI) occurs when a traumatic event causes the brain to move rapidly within the skull, leading to damage. As illustrated in the poster (panel A), the event can be classified as either impact or non-impact, depending on whether the head makes direct contact with an object (impact) or encounters a non-impact force such as blast waves or rapid acceleration and deceleration.
Traumatic Brain Injury Epidemiology and Pathophysiology March 10, 2017 Cherry Junn, M.D. Pinella Holder, D.O. University of Washingto Traumatic brain injury continues to be a critical health and socioeconomic problem worldwide across low and high-income countries due to its life-long consequences and as it can affect people at any age. Socioeconomic change in low and middle-income countries due to urbanisation and mechanisation also drives an increase in traumatic brain injury in these regions. One study found that TBI was. . As the primary injury cannot be undone, management strategies must therefore focus on preventing secondary injury by avoiding hypotension and hypoxia and maintaining appropriate cerebral perfusion pressure (CPP), which is a surrogate for cerebral blood flow (CBF) Animal models of traumatic brain injury have included fluid percussion injury , controlled cortical impact injury (23,24) and weight-drop impact acceleration injury . Microwave exposure of 3.2 kW caused cerebral contusion in the cortex. Although this level of microwave exposure showed no effect on the body surface, cranium, brain surface or cortex, it caused changes deep in the brain. The.
Photophobia: shared pathophysiology underlying dry eye disease, migraine and traumatic brain injury leading to central neuroplasticity of the trigeminothalamic pathway. British Journal of Ophthalmology, Vol. 105, Issue. 6, p. 751 Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition, and the AANS and CNS leadership for their endorsement, which appears on the title page. Funding Source . This material is based in part upon work supported by (1) the U.S. Army Contracting Command, Aberdeen Proving Ground, Natick Contracting Division, through a contract awarded to Stanford University (W911 QY-14-C. Small interfering RNA (siRNA) represents a powerful strategy to mitigate the long-term sequelae of traumatic brain injury (TBI). However, poor permeability of siRNA across the blood brain barrier (BBB) poses a major hurdle. One approach to overcome this challenge involves treatment administration while the BBB is physically breached post-injury
Pathophysiology of microwave-induced traumatic brain injury Biomed Rep. 2015 Jul;3(4):468-472. doi: 10.3892/br.2015.454. Epub 2015 Apr 29. Authors Yutaka Igarashi 1. traumatic brain injury (TBI), with an overall mortality rate of 29%.1 In a recent study by Kamal et al,2 out of 1,527 patients with moderate to severe TBI admitted to All India Institute of Medical Sciences, New Delhi, mortality was 34% and remain - ing 67% had an unfavorable outcome at 6 months.2 Mortality due to TBI is often related to direct injury to the brain and its consequences of. Pathophysiology Diagram Of Traumatic Brain Injury Free Books [READ] Pathophysiology Diagram Of Traumatic Brain Injury PDF Book is the book you are looking for, by download PDF Pathophysiology Diagram Of Traumatic Brain Injury book you are also motivated to search from other sources REVIEW Open Access Traumatic Brain Injury: PathophysiologyIs To Maintain A Continuous Cerebral Blood Flow. Cerebral Edema in Traumatic Brain Injury: Pathophysiology and Prospective Therapeutic Targets Ethan A. Winkler, Daniel Minter, John K. Yue, Geoffrey T. Manley Pages 473-48
Traumatic brain injury (TBI), defined as brain damage caused by externally inflicted trauma to the head, may result in significant impairment of an individual's functioning— physical, cognitive, and psychosocial. In the United States, an estimated 1.5 to 2 million people incur TBI each year, principally as a result of automobile crashes, sports accidents, falls, and acts of violence. The. Memory is fundamental to everyday life, and cognitive impairments resulting from traumatic brain injury (TBI) have devastating effects on TBI survivors. A contributing component to memory impairments caused by TBI is alteration in the neural circuits associated with memory function. In this review, we aim to bring together experimental findings that characterize behavioral memory deficits and. Traumatic brain injury (TBI) is a major source of health loss and disability worldwide. Globally, the annual incidence of TBI is variably estimated at 27 to 69 million [ 1,2 ]. Many survivors live with significant disabilities, resulting in major socioeconomic burden. In 2010, the economic impact of TBI in the United States was estimated to be. The latest French Guidelines for the management in the first 24 hours of patients with severe traumatic brain injury (TBI) were published in 1998.Due to recent changes (intracerebral monitoring, cerebral perfusion pressure management, treatment of raised intracranial pressure), an update was required Traumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury, causes substantial disability and mortality. It occurs when a sudden trauma damages the brain and disrupts normal brain function. TBI may have profound physical, psychological, cognitive, emotional, and social effects. Mild TBI appears to be vastly underdiagnosed in the setting of systemic trauma.
Pathophysiology of Traumatic Brain Injury Kirsty J. Dixon, PhD TRAUMATIC BRAIN INJURY: CAUSES, PREVALENCE, AND DEVELOPMENT OF THE NATIONAL RESEARCH ACTION PLAN Traumatic brain injury (TBI) may have many different causes, including a blow to the head, penetration of the skull, fast acceleration or deceleration of the head, or expo- sure to a blast. In the United States, there are more than 5.3. Traumatic brain injury (TBI) remains one of the most complex diseases known in the most complex of all organs in the body. The causes of TBI are many and varied and include penetrating and nonpenetrating injuries that, based on their overall level of severity, can evoke different degrees of morbidity, typically framed within the context of the Glasgow Coma Scale (GCS) score The Pathophysiology of Traumatic Brain Injury (TBI): A Review Download-PDF The Pathophysiology of Traumatic Brain Injury (TBI): A Review Download-PDF. Thumbnails Document Outline Attachments. Previous. Next. Highlight all Match case. Presentation Mode Open Print Download Current View. Go to First Page Go to Last Page. Rotate Clockwise Rotate Counterclockwise. Enable hand tool. Document. Traumatic brain injury (TBI), which is defined as a physical injury to brain tissue that temporarily or permanently impairs brain function, is a global health concern and a growing socioeconomic problem. TBI is the leading cause of mortality and disability among individuals under the age of 45, with young adult males accounting for approximately 75% of cases. Due to the complex pathophysiology. Traumatic brain injury triggers a complex and interwoven sequence of ionic and metabolic events from which damaged cells may eventually recover or, in certain circumstances, degenerate and die. Brain concussion triggers a multi-layered neurometabolic cascade of physiologic changes that has important implications for cerebral vulnerability, cell death, plasticity and persistent neurocognitive.
Traumatic brain injury continues to be a major socioeconomic problem, costing the United States $76.5 billion in the year of 2000. Despite the advances in the field of medicine, there are still no definitive treatments for traumatic brain injury.Goal of therapy is still gearing toward supportive cares such as intracranial pressure monitoring, lowering intracranial pressure, correcting cerebral. Juškys R, Hendrixson V. Pathophysiology of severe traumatic brain injury and management of intracranial hypertension. LS [Internet]. 2019Jul.9 [cited 2021Jun.13];18(2):62-1
Treatment of traumatic brain injury pdf A variety of treatments can help a person recover from TBI and can sometimes reduce or eliminate certain physical, emotional, and cognitive problems associated with TBI. The specifics of treatment, including the type, setting, and length, depend on how severe the injury is and the area of the brain that was injured. Close Citations National Institute of. PDF NANDA I 2018 2020 pdf herry setiawan Academia edu April 8th, 2019 - NANDA I 2018 2020 pdf Herry Setiawan Download with Google Download with Facebook or download with email Imaging of Spinal Cord Injury Acute Cervical Spinal Cord April 19th, 2019 - We review the pathophysiology and imaging findings of acute traumatic spinal cord injury SCI cervical spondylotic myelopathy and briefly review. There are 2 million cases of traumatic brain injury (TBI) per year in the US, many of which require in-hospital treatment including either surgical intervention or close observation. TBI is classified as mild, moderate or severe based on the Glasgow Coma Score (GCS). Severe TBI, accounts for 10% of all TBI, is defined as a GCS of less than 9 and has a mortality rate of close to 40%. Moderate. Pathophysiology and treatment of traumatic brain edema Abhishek Patro MBBS, Sureswar Mohanty M Ch Department of Neurosurgery IMS & SUM Hospital, Bhubaneswar-751003 Abstract:Traumatic brain edema is a secondary phenomenon of traumatic brain injury. It manifests during a time interval by escape of fluid from the vascular compartment to extracellular spaces (vasogenic edema) or due to failure of. Traumatic Brain Injury, Fourth Edition The scope and purpose of this work is 2-fold: to synthesize the available evidence and to translate it into recommendations. This document provides recommendations only when there is evidence to support them. As such, they do not constitute a complete protocol for clinical use. Our intention is that these recommendations be used by others to develop.
Pathophysiology of the traumatic brain injury and post-traumatic hypopituitarism iago Pereira Rodrigues 1, Marcos Antônio Dias 2, Alexandre Hohl 3*, Tânia Longo Mazzuco 4* Resumo O traumatismo crânio-encefálico (TCE) é um problema sério de saúde pública em todo o mundo, devido às incapacidades funcionais decorrentes de lesões traumáticas. Esta revisão aborda a biomecânica do TCE. The Textbook of Traumatic Brain Injury is a must-read for all of those working in any of the multitude of disciplines that contribute to the care and rehabilitation of persons with brain injury. This new volume is also a potentially useful reference for policymakers in both the public and private sectors. Contents. Foreword; Preface; Part I: Epidemiology and Pathophysiology; Chapter 1.
Pathophysiology Diagram Of Traumatic Brain Injury ideadiez com, well the new york times, imaging of spinal cord injury acute cervical spinal cord, chapter 42 heat and cold ilocis org, epidural hematoma wikipedia, managing the psychiatric crisis national center of, thoracic trauma management of hemothorax and blunt, pathophysiology and treatment of cerebral edema in, george washington. The Journal of Head Trauma Rehabilitation is a leading, peer-reviewed resource that provides up-to-date information on the clinical management and rehabilitation of persons with traumatic brain injuries. Six issues each year aspire to the vision of knowledge informing care and include a wide range of articles, topical issues, commentaries and special features TBI pathophysiology and existing and potential new therapeutic strategies in the management of inﬂammatory events and behavioral deﬁcits associated with TBI. Keywords: neuroinﬂammation; traumatic brain injury; palmitoylethanolamide (PEA); therapeutic strategies; oxidative stress. 1. Introduction Traumatic brain injury (TBI) is deﬁned as damage to the brain sustained after the.
Narrative Review of the Pathophysiology of Headaches and Photosensitivity in Mild Traumatic Brain Injury and Concussion Christopher Mares, Jehane H. Dagher, Mona Harissi-Dagher ABSTRACT: The most common symptom of post-concussive syndrome (PCS) is post-traumatic headache (PTH) accompanied by photophobia.Post-traumaticheadacheiscurrently. Traumatic brain injury (TBI) represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death The Traumatic Brain Injury Act of 2008 authorized research and public health activities related to traumatic brain injury (TBI). The goal of public health related to injury prevention is to reduce the burden of injury at the population level by preventing injuries and ensuring care and rehabilitation that maximizes the health and quality of life for injured persons. The purpose of this report Mild traumatic brain injury (mTBI) or sport-induced concussion has recently become a prominent concern not only in the athletic setting (i.e. sports venue) but also in the general population. The majority of research to date has aimed at understanding the neurological and neuropsychological outcomes of injury as well as return-to-play guidelines. Remaining relatively unexamined has been the.
Traumatic brain injury (TBI) accounts for about 30-50% of all trauma-related deaths with a male predominance . It can be classified on the basis of neurological assessment using Glasgow Coma Score into, mild (13/15), moderate (9-12/15) and severe (3-8/15). Moderate to severe TBI often require admission to the Intensive care unit (ICU). The aetiology of TBI includes but not limited to road. RESEARCH ARTICLE Nervous System Pathophysiology Phosphorylation of connexin 43 induced by traumatic brain injury promotes exosome release Wei Chen, Yijun Guo, Wenjin Yang, Lei Chen, Dabin Ren, Chenxing Wu, Bin He, Ping Zheng, and Wusong Tong The People's Hospital of Pu Dong New Area, Chuansha New Town, Shanghai, People's Republic of China Submitted 4 September 2017; accepted in ﬁnal form. management of mild traumatic brain injury, or con-cussion. Clinical care of athletes with concussion has traditionally centered on recognizing signs and symp-toms associated with a concussive event. Over the last 2 decades, the catag of concussive manifestations into tiered grading scales has allowed identification and ultimate management of those injured, to guide their proper recov-ery. Introduction. Traumatic brain injury (TBI) is a major cause of mortality and morbidity. In England and Wales, ∼1.4 million patients per year attend hospital following head injury and it is the most common cause of death under the age of 40 years.1 Over the past 30 years, advances in management including the introduction of Advanced Trauma Life Support2 National Institute for Health and Care.
Traumatic Brain Injury. Edited by: Farid Sadaka. ISBN 978-953-51-1222-8, PDF ISBN 978-953-51-7192-8, Published 2014-02-19 . Traumatic brain injury is a major source of death and severe disability worldwide. This book provides an excellent and detailed overview of the management of patients with traumatic brain injury, in a stepwise approach, from the intensive care unit, through to discharge. Traumatic brain injury (TBi) is the leading cause of death and disability in children. TBi in children result in a range of traumatic injuries to the scalp, skull, and brain that are comparable to those in adults but differ in both pathophysiology and manage-ment. The differences are attributable to age-relate Traumatic brain injury (TBI) leads to increased rates of dementia, including Alzheimer's disease. The mechanisms by which trauma can trigger neurodegeneration are increasingly understood. For example, diffuse axonal injury is implicated in disrupting microtubule function, providing the potential context for pathologies of tau and amyloid to develop ognizes that the pathophysiology of traumatic brain in-jury evolves over time, and treatment that is appropriate in the ﬁrst few hours after injury may not necessarily be optimal 2 or 3 days after injury. Miller et al.6 proposed that treatment of intracranial hypertension was more successful if the treatment was targeted at the underly-ing cause, i.e., hypnotic-sedative agents for vascular.
Keywords: traumatic brain injury; stem cells; clinical studies; clinical trials; stem cell transplantation 1. Introduction TBI is a leading global cause of mortality and morbidity [1,2] and the main cause of death in young people living in industrialized countries . TBI is mainly caused by an external mechanical force causing brain trauma. This trauma can lead to temporary or permanent. Traumatic brain injury (TBI; see Box 1 for a glossary of terms) is a leading cause of death and disability worldwide, particularly for persons under 45 years of age (Hyder et al., 2007; Mass et al., 2008).In the United States, the overall incidence of TBI is estimated to be 538 per 100,000 individuals, which represents at least 1.7 million new cases per year since 2003 (Gerberding and Binder.
Traumatic brain injury (TBI) is a leading cause of mortality and morbidity both in civilian life and on the battlefield worldwide. Animal models are essential for studying the biomechanical. The diagnosis of mild traumatic brain injury (MTBI) is a good example of severity of TBI based on multiple acute injury indices. These include the Glasgow Coma Scale, length of post-traumatic amnesia, results of neuroimaging and focal signs. The American Congress of Rehabilitation Medicine, Centre for Disease Control, and the World Health Organisation include the criterion for a MTBI as: loss. After severe traumatic brain injury, medical and surgical therapies are performed to minimize secondary brain injury. 7-9 Increased intracranial pressure, which is typically caused by cerebral. Traumatic brain injury is usually caused by a blow or other traumatic injury to the head or body. The degree of damage can depend on several factors, including the nature of the injury and the force of impact. Common events causing traumatic brain injury include the following: Falls. Falls from bed or a ladder, down stairs, in the bath, and other falls are the most common cause of traumatic.