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. Key differences between olfactory ensheathing cells and Schwann cells regarding phagocytosis of necrotic cells: implications for transplantation therapies. Apoptotic and necrotic neurons are present even in mild injuries and can be found in areas distant from the injury impact area. 2016 Oct;27(4):473-88. doi: 10.1016/j.nec.2016.05.008. 2007 (1): 4–9 doi:10.1093/bja/aem131. Brainline. The cascade of mismatched processes of overflow and metabolism creates excitotoxicity. Traumatic brain injury (TBI) of any sort can … More-serious traumatic brain injury can result in bruising, torn tissues, bleeding and other physical damage to the brain. Introduction • Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. Studies in laboratory animals and humans have investigated the effects of TBI on CBF. After major brain injury, brain temperature is often higher than and can vary independently of systemic temperature. The blood brain barrier becomes impaired and white matter injury usually increases. When refering to evidence in academic writing, you should always try to reference the primary (original) source. The major topics in SAH research focus on early brain injury and delayed cerebral ischemia causing neurological deficits and bad outcome. Definition Traumatic brain injury is a non degenerative, non congenital insult to the brain from an external mechanical force ,possibly leading to permanent or temporary impairment of cognitive, physical and psychosocial functions, with an associated diminished or altered state of consciousness 3. Damage to blood vessel endothelium following TBI triggers a neuroinflammation process with a release of cytokines, free radicals, prostaglandins and complements mobilising an active response from immune system to eliminate the damaged cells and format scar tissue. Curr Neuropharmacol. Cytotoxic oedema results from intracellular water accumulation related to increased cell membrane permeability. There are many different definitions of Acquired Brain Injury - the “acquired” bit refers to any damage to the brain that occurs after birth, and is meant to differentiate brain injury from congenital disabilities like intellectual disability - and, doubtless, none of them are perfect in, for example, what conditions or diseases they include or exclude. Several groups of proteins and biochemical transitional pathways are involved in cell death mechanisms and their tracking might create new therapeutic opportunities limiting neurodegeneration and resulting disabilities especially with apoptosis providing the window of opportunity for therapy due to its delayed nature. Initial treatment consists of ensuring a reliable airway and maintaining adequate ventilation, oxygenation, and blood pressure. J Neurosurg 27:1–11. A TBI can cause you to lose consciousness, have amnesia for a while, or be confused for weeks. Cerebral oxygenation. Brain Injury is the “multiple disabilities arising from damage to the brain acquired after birth. Immediately following mTBI, there are several metabolic, hemodynamic, stru … Further damage may occur shortly thereafter from the cascade of events triggered by the initial injury. Pathophysiology of traumatic brain injury By Amir Rezagholizadeh 2. The Glasgow Coma Scale(GCS) is the mainstay for rapid neurologic assessment in acute head injury. While our understanding of these mechanisms has advanced greatly over the last decade, there is still much to learn and great uncertainty at the bedside. In this review we summarize the current understanding of mechanisms and pathophysiology of primary and secondary brain injury, the goals for current treatment and potential targets for future therapy. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). Traumatic Brain Injury: Outcome and Pathophysiology . 2020;18(3):188-201. doi: 10.2174/1570159X17666191010103044. Traumatic brain injuries are usually emergencies and consequences can worsen rapidly without treatment. A. Chodobski, B.J. Therefore, measuring brain oxygenation is one of the standard measurements along with ICP and CPP. USA.gov. An object that penetrates brain tissue, such as a bullet or shattered piece of skull, also can cause traumatic brain injury.Mild traumatic brain injury may affect your brain cells temporarily. COVID-19 is an emerging, rapidly evolving situation. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. The main mechanism involved in maintaining consistent cerebral pressure in response to changing systemic arterial pressure are vasoconstriction and vasodilatation of brain vessels. Bruising or bleeding on the head and scalp and blood in the ear canal or behind the tympanic membranes: May be clues to occult brain injuries 2. The World Health Organization (WHO) estimates that more than five million people die each year from traumatic injuries worldwide. Trends in Neuroscience. Using 133 Xe scintillation detection, 133 Xe computed tomography (CT), stable xenon CT, or 15 O 2 positron emission CT to assess CBF within a temporal range from ultra-early to late stages after TBI, … The quick back-and-forth can cause a brain injury. DOI 10.1186/s40560-016-0138-3, Werner C., Engelhard K. Pathophysiology of traumatic brain injury. Secondary brain injury occurs at a time after the initial mechanical trauma. This cascade might result in oedema formation, increase of intracranial pressure (ICP), and decreased cerebral perfusion pressure (CPP). Neurosurg Clin N Am. Physiopedia is not a substitute for professional advice or expert medical services from a qualified healthcare provider. Read more, © Physiopedia 2020 | Physiopedia is a registered charity in the UK, no. A traumatic brain injury (TBI), also known as an intracranial injury, is an injury to the brain caused by an external force. Multiple factors can initiate these vasodilation or vasoconstriction cascades, including; [4]. Chronic Pain After Traumatic Brain Injury: Pathophysiology and Pain Mechanisms. Primary brain injury The primary impact to the brain and skull may cause bony fractures, intracranial haematomas, brain contusion, axonal injury and disruption of the blood-brain barrier. The normal range of this difference is between 50 and 70 mmHg. Pathophysiology of traumatic brain injury By Amir Rezagholizadeh 2. Key points of the “pathophysiology for neurocritical care” in traumatic brain injury Cerebral autoregulation is one of the important pressure reactivity systems in the brain. Excitotoxicity and oxidative stress. The oxidative stress related to imbalance of free radicals and endogenous antioxidants availability can lead to immediate cell death or inflammatory processes or apoptosis. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). Traumatic brain injury is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile. Diagnosis is suspected clinically and confirmed by imaging (primarily CT). doi: 10.1002/14651858.CD009986.pub2. Due to reduced proximal cerebrovascular resistance and increased cerebral blood volume and vessel dilatation the impaired brain blood barrier causes an excess of fluids to reside in vascular bed. The disability called brain injury – sometimes called acquired brain injury, or “ABI” – refers to any damage to the brain that occurs after birth. Brain function is temporarily or permanently impaired and structural damage may or … [1] Multiple factors contribute to those pathophysiological mechanisms of secondary injury and their contribution to the severity of the secondary injury might vary. 1173185, Hill CS, Coleman MP, Menon DK. At the time of impact, the primary brain injury results in neuronal, vascular, and glial damage. Oedema is a common result of traumatic brain injury and can be vasogenic or cytotoxic and can cause ICP increase and secondary ischemia. Traumatic Brain Injury (TBI) is an injury to the brain caused by a trauma to the head (head injury). Traumatic brain injury (TBI) of any sort can … Diagnosis is suspected clinically and confirmed by imaging (primarily CT). Initial treatment consists of ensuring a reliable airway and maintaining adequate ventilation, oxygenation, and blood pressure. Recent Advances in Pathophysiology of Traumatic Brain Injury. Authors; Authors and affiliations; Konstantina A. Svokos; Amir Kershenovich; Chapter. The World Health Organization (WHO) estimates that more than five million people die each year from traumatic injuries worldwide. Necrosis (cell death) occurs after the first few hours following an insult to brain tissue, mechanical or hypoxic, and is related to cell membrane damage and uncontrolled release of cell death products. 2016 Oct;27(4):509-17. doi: 10.1016/j.nec.2016.05.010. Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. 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. "Introduction to Traumatic Brain Injury" by Lisa DelSignore, MD for OPENPediatrics. TBI presents a significant health issue in the United States, with more than 2.5 million cases resulting in emergency department visits, hospitalizations or fatality [].Furthermore, memory impairment is one of the most common neurological manifestations of TBI [2–4]. Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. National Center for Biotechnology Information, Unable to load your collection due to an error, Unable to load your delegates due to an error. Abstract Traumatic brain injury (TBI) is named the most complex disease in the most complex organ in the body. Abnormal postresuscitation pupillary reactivity: Correl… 2016. A head injury is an injury to your brain, skull, or scalp. Some brain injuries cause focal -- or localized -- brain damage, such as the damage caused when a bullet enters the brain. OPENPediatrics. Traumatic brain injury (TBI) is one of the most common injuries sustained on current non-linear battlefields. In other words, the damage is confined to a small area. E-mail: werner@anaesthesie.klinik.uni-mainz.de The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. Therefore, decreased CBF with a normal metabolic rate creates ischemic conditions. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Head injury can be defined as any alteration in mental or physical functioning related to a blow to the head (see the image below). Neurological presentation of Diffuse Axonal Injury includes bilateral neurological examination deficits frequently affecting the frontal and temporal white matter, corpus callosum, and brainstem. Aronowski J(1), Zhao X. These injuries can result in long-term complications or death. Following ascertainment of the GCS score, the examination is focused on signs of external trauma, as follows: 1. Secondary brain injury Secondary brain injury occurs as a consequence of cerebral ischaemia and inflammatory and cytotoxic processes. Cerebral Edema in Traumatic Brain Injury: Pathophysiology and Prospective Therapeutic Targets. Pathophysiology of TBI Damages of neuronal tissues associated with TBI fall into two categories: (i) primary injury, which is directly caused by mechanical forces during the initial insult; and (ii) secondary injury, which refers to further tissue and cellular damages following primary insult. Zink, J. Szmydynger-ChodobskaBlood-brain barrier pathophysiology in traumatic brain injury Transl. Vasogenic brain oedema is caused by endothelial cells damage. This can range from a mild bump or bruise to a traumatic brain injury. It results in deterioration in cognitive, physical, emotional or independent functioning. Noppens R, Brambrink AM. That is usually the journal article where the information was first stated. TBI is extremely heterogeneous and so is the underlying pathophysiology. This pathology is equally detrimental to brain tissue as ischemia causing an increase in intracranial pressure. Pathophysiology of Brain Injury. Curr Neuropharmacol. Proinflammatory enzymes like interleukin-1, interleukin -6 intensify the activity within the first hours from initial insult. Degenerating oligodendrocytes and astrocytes are present in the white matter of primary injury area. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. Traumatic brain injury (TBI) is defined as any force to the head that causes alteration in neurological function. Pathophysiology Brain function may be immediately impaired by direct damage (eg, crush, laceration) of brain tissue. 2019 Sep 26;24(19):3502. doi: 10.3390/molecules24193502. The resulting detritus is interpreted as an ‘antigen’ and triggers inflammatory process and scaring. Outline • Introduction • Etiology • Classification • Symptoms • General pathophysiology of TBI • Specific pathophysiology of TBI • References 3 4. J Neurosurg 27:1–11. Oedema. Traumatic brain injury impairs or even abolishes cerebrovascular autoregulation immediately after the trauma or over time. Cerebral metabolic disfunction relates to oxygen and glucose depletion as well as reduced cerebral energy state at the period of post traumatic hypermetabolic demand. A Mechanistic Rationale for PDE-4 Inhibitors to Treat Residual Cognitive Deficits in Acquired Brain Injury. Severe cases of traumatic brain injury (TBI) require neurocritical care, the goal being to stabilize hemodynamics and systemic oxygenation to prevent secondary brain injury. The primary insult of axonal injury leads to disconnection and/or neuron connections malfunction resulting in functional areas impairment. The more severe the injury with extensive secondary damage, the less possible axonal reconnection and function recovery. The ion and protein flow through vascular walls to interstitial space causing an increased volume in extracellular space. [6] The overload of excitatory amino acid neurotransmitters results in overstimulation of ionotropic and metabotropic glutamate receptors with consecutive calcium, sodium and potassium ions flow triggering brain blood barrier breakdown and cellular compensatory ATPase activity increase resulting in aggravated metabolic demand. Reference 2 3. CrossRef Google Scholar 2004 Oct. 56(1-2):113-25. . Traumatic brain injury usually results from a violent blow or jolt to the head or body. Traumatic brain injury (TBI) is a major cause of death and disability in the United States. Further damage may occur shortly thereafter from the cascade of events triggered by the initial injury. The imbalance of pro and anti-apoptotic proteins triggers the cell death mechanism hours post primary insult. Traumatic brain injury is a leading cause of morbidity and mortality globally, particularly among young people, with significant social and economic effects. While public health initiatives such as seatbelts and airbags have had a major impact, it will be impossible to prevent traumatic brain injury.Therefore, it is important that we understand the pathophysiology of secondary brain injury to be able to effectively treat our patient and also to develop novel targets of future interventions. Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. Understanding Diffuse Axonal Injury. 2018 Jul 1;19(7):1315-1333. doi: 10.1093/pm/pnx153. [6] Coexisting traumatic damage such as structural injury of cell bodies, astrocytes and microglia, cerebral vascular and endothelial damage intensify the brain tissue damage. Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of … Anosmia: Common; probably caused by the shearing of the olfactory nerves at the cribriform plate[3] 3. Clinical outcomes depend in large part on mediating the bimolecular and cellular changes that occur after the initial injury. TBI metabolic failure is also related to imbalance between oxygen supply and oxygen consumption and leads to hypoxia. Available from: I give my consent to Physiopedia to be in touch with me via email using the information I have provided in this form for the purpose of news, updates and marketing. There are many possible causes, including road traffic accidents, assaults, falls and accidents at … Cerebral blood flow. TBI is classified according to its severity: mild, moderate or severe. Common events causing traumatic brain injury include the following: Falls. Closed head injuries frequently cause diffuse brain damage, which means damage to several areas of the brain. Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. First Online: 13 May 2014. The leucocytosis increasing cell debris and phagocytosis response may further increase the inflammatory response and tissue destruction affecting undamaged tissue extending the injury and decomposing dead tissue. The Adams Diffuse Axonal Injury Classification: A mild diffuse axonal injury with microscopic white matter changes in the cerebral cortex, corpus callosum, and brainstem, A moderate diffuse axonal injury with gross focal lesions in the corpus callosum. The extent of the hypoxia and its duration determines the clinical outcome. The Monroe Kellie Hypothesis Before moving on to the pathophysiology of secondary brain injury, it is important to understand a few key concepts and definitions. Traumatic brain injury (TBI) is one of the most prevalent causes of morbidity and mortality all over the world. A nonlinear battlefield describes an area of military operations where there is a less precise structure and close operations (combat) can take place throughout the entire area. Concussion or mild traumatic brain injury (mTBI) is a condition that affects hundreds of thousands of patients worldwide. Reference 2 3. Focal & diffuse brain injury A TBI can be focal or diffuse, meaning damage may be isolated to one specific area of the brain, or widespread. Secondary brain injury is what occurs as a result of the primary injury secondary to the pathophysiological process of inflammation within the brain. Primary brain injury, due to initial injury forces, causes tissue distortion and destruction in the early postinjury period. Whereas primary brain injury (focal and diffuse) results from mechanical injury at the time of the trauma, secondary brain injury is caused by the physiologic responses to the initial injury. The normal brain vascular autoregulation includes a pressure and volume monitoring mechanism allowing continuous cerebral blood flow (CBF) and optimal oxygen supply. Vascular-related changes (barrier breakdown, vasospasm, oedema) HHS The extent of deafferentation in mild to severe injuries and axonal damage impacts the ability of synaptic sprouting of undamaged axons. The mechanism responsible for oedema formation and intracranial pressure increase is hyperaemia. Molecular pathophysiology of cerebral hemorrhage: secondary brain injury. Specific pathophysiology of traumatic brain injury Cerebral blood flow Hypoperfusion and hyperperfusion. Harrison-Felix C, Whiteneck G, Devivo MJ, et al. Common causes include falls, car accidents, assault or being struck by objects such as might occur during sport. Available from: Kinoshita K. Traumatic brain injury: pathophysiology for neurocritical care. While public health initiatives such as seatbelts and airbags have had a major impact, it will be impossible to prevent traumatic brain injury.Therefore, it is important that we understand the pathophysiology of secondary brain injury to be able to effectively treat our patient and also to develop novel targets of future interventions. Following an initial insult, an ischemia like stage of traumatic brain injury triggers a cascade of processes characterised by direct brain tissue damage and cerebral blood flow (CBF) regulation impairment as well as metabolism impairment. Introduction. Alarcon JD, Rubiano AM, Okonkwo DO, Alarcón J, Martinez-Zapata MJ, Urrútia G, Bonfill Cosp X. Cochrane Database Syst Rev. Apoptosis is triggered by cell surface receptor engagement, growth factor withdrawal and DNA damage. Traumatic brain injury (TBI) is named the most complex disease in the most complex organ in the body.  |  There has been some recent success with the discovery of some simple interventions that can reduce secondary brain injury and improve outcomes in patients after traumatic brain injury. https://www.physio-pedia.com/index.php?title=Pathophysiology_of_Traumatic_Brain_Injury&oldid=254698, Cortical and subcortical neuronal injury/death, Vascular-related changes (barrier breakdown, vasospasm, oedema), Depolarisation and disturbance of ionic homeostasis, Neurotransmitter release (e.g. Sci Rep. 2020 Nov 3;10(1):18936. doi: 10.1038/s41598-020-75850-8. Definitions of Brain Injury. Pain Med. Cerebral metabolic dysfunction. TBI is extremely heterogeneous and so is the underlying pathophysiology. Both hypoperfusion and hyperperfusion is related to the difference between cerebral blood flow and cerebral metabolism and oxygen consumption. The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. 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. Outline • Introduction • Etiology • Classification • Symptoms • General pathophysiology of TBI • Specific pathophysiology of TBI • References 3 4. Clipboard, Search History, and several other advanced features are temporarily unavailable. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. General pathophysiological features of traumatic brain injury and mechanism following primary onset might include: These pathophysiological events impair cell function impacting movement, memory and learning ability as well as potentially causing damage to white matter structure. This is called diffuse axonal injury or DAI. 4:29-39. 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. Cerebral ischemia is a state of decreased blood supply of the brain (hypoperfusion) and leads primarily to metabolic stress and ionic perturbations. The initial traumatic injury to brain tissue is defined as the primary brain injury. Fehér E, Szatmári I, Dudás T, Zalatnai A, Farkas T, Lőrinczi B, Fülöp F, Vécsei L, Toldi J. Molecules. Understanding the pathophysiology of this disorder can help manage its acute and chronic repercussions. The factors involved in post-traumatic vasospasm and contributing to resultant ischaemia include: TBI frequently leads to focal or global cerebral ischemia and its presence points towards poor clinical outcome like persistent vegetative state or death. Pathophysiology Brain function may be immediately impaired by direct damage (eg, crush, laceration) of brain tissue. If you believe that this Physiopedia article is the primary source for the information you are refering to, you can use the button below to access a related citation statement. The degree of damage can depend on several factors, including the nature of the injury and the force of impact. That damage can be caused by an accident or trauma, by a stroke, by a brain infection, by alcohol or other drug abuse or by diseases of the brain … However, CT Head has a low yield in detecting Diffuse Axonal Injuries and Magnetic Resonance Imaging (MRI), specifically Diffuse Tensor Imaging (DTI), is the imaging modality of choice for diagnosis of diffuse axonal injury. Traumatic brain injury is usually caused by a blow or other traumatic injury to the head or body. Mechanically disrupted axons present cytoskeletons malfunction resulting in proteolysis, swelling, and other microscopic and molecular changes to the neuronal structure. Cerebral perfusion pressure is the difference between the systemic arterial pressure and the intracranial pressure. The Role of Multimodal Invasive Monitoring in Acute Traumatic Brain Injury. In intensive care clinical practice, the continuous monitoring of core temperature in patients with brain injury is currently highly recommended. Traumatic brain injury (TBI) is an injury to the brain caused by an external force. Title:Recent Advances in Pathophysiology of Traumatic Brain Injury VOLUME: 16 ISSUE: 8 Author(s):Parmeet Kaur and Saurabh Sharma* Affiliation:Department of Pharmacology, I.S.F College of Pharmacy, Moga-142001, Punjab, Department of Pharmacology, I.S.F College of Pharmacy, Moga-142001, Punjab Keywords:Traumatic brain injury, secondary injury, primary brain injury, oxidative … Elevation of the head during intensive care management in people with severe traumatic brain injury. Top Contributors - Naomi O'Reilly, Rachael Lowe, Kim Jackson and Tony Lowe. Available from: Brainline. 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. Nazareth L, Shelper TB, Chacko A, Basu S, Delbaz A, Lee JYP, Chen M, St John JA, Ekberg JAK. Primary traumatic brain injury insult triggers complex cellular and molecular processes leading to further neuronal dysfunction and death (secondary injury). 39(5): 311-324 doi.org/10.1016/j.tins.2016.03.002, Bouzat P, Sla N, Payen JF, Oddo M. Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury. 2.5k Downloads; Abstract . Pathophysiology of traumatic brain injury C. Werner* and K. Engelhard Klinik fu¨r Ana¨sthesiologie, der Johannes Gutenberg-Universita¨t Mainz, Langenbeckstrasse 1, D-55131 Mainz, Germany *Corresponding author. The observation that brain cells are more resistant to ischemia than was previously assumed on the basis of clinical experience has stimulated considerable investigative work designed to determine those factors responsible for irreversible ischemic cell damage. Traumatic brain injury is a leading cause of morbidity and mortality globally, particularly among young people, with significant social and economic effects. Focus on outcome from traumatic brain njury . The variety of processes involved contributes to the traumatic brain injury complexity but also creates various therapeutic targets. NIH The mechanisms of secondary brain injury are complex involving alterations in cerebral perfusion, activation of inflammatory cytokines and excitotoxicity. Data suggest that the different types and severities of TBI have unique long-term outcomes and thus may represent different types of diseases. Causes of death following 1 year postinjury among individuals with traumatic brain injury. The following clinical mechanisms contribute to the dysregulation of the mechanisms that usually maintain volume and pressure: Cerebral blood flow (CBF) disruption can also be caused by mechanical displacement of brain structures, stretching and distorting brain vessels, arterial hypotension, vasospasm, changes in cerebral microvasculature. 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. Common causes of secondary brain injury may include hypoxia, hypotension, increased intracranial pressure (ICP) or … J Head Trauma Rehabil . This is thought to involve a cascade of events, with edema and hematomas leading to increased intracranial pressure, which leads to compression and deformation of surrounding brain tissue and further damage. Cerebral ischaemia The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. Words, the content on or accessible through Physiopedia is for informational purposes only blood pressure Nov ;! Concussion or mild traumatic brain injury ( TBI ) is one of the pathophysiology after traumatic injury!:188-201. doi: 10.2174/1570159X15666170613083606 mediating the bimolecular and cellular changes that occur after the initial trauma... E-Mail: Werner @ anaesthesie.klinik.uni-mainz.de the knowledge of the complex pathophysiology of traumatic injury... Increase and secondary ischemia or be confused for weeks with cerebral blood flow following CA undamaged.! 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