The excessive production of reactive oxygen species due to excitotoxicity and exhaustion of the endogenous antioxidant system (e.g. In contrast, neurons undergoing apoptosis are morphologically intact during the immediate post-traumatic period with adequate ATP-production providing a physiological membrane potential. These processes induce chemokines and adhesion molecules and in turn mobilize immune and glial cells in a parallel and synergistic fashion.Two different types of cell death may occur after TBI: necrosis and apoptosis (programmed cell death). Understanding the multidimensional cascade of injury offers therapeutic options including the management of CPP, mechanical (hyper-) ventilation, kinetic therapy to improve oxygenation and to reduce ICP, and pharmacological intervention to reduce excitotoxicity and ICP.
Search for other works by this author on: However, there is a paucity of information regarding the effect of TBI on cerebral autoregulation in children. Absolute differences, temporal changes, and association with outcome of the 2 indices were analyzed.A total of 486 recording sessions obtained from 201 patients were available for analysis. If you originally registered with a username please use that to sign in. The current classification of brain oedema relates to the structural damage or water and osmotic imbalance induced by the primary or secondary injury. This review consolidates the current pathophysiological view of TBI predominantly derived from clinical work with particular emphasis on cerebral blood flow (CBF) and metabolism, cerebral oxygenation, excitotoxicity, oedema formation, and inflammatory processes.The principal mechanisms of TBI are classified as (a) focal brain damage due to contact injury types resulting in contusion, laceration, and intracranial haemorrhage or (b) diffuse brain damage due to acceleration/deceleration injury types resulting in diffuse axonal injury or brain swelling.The first stages of cerebral injury after TBI are characterized by direct tissue damage and impaired regulation of CBF and metabolism.
Copyright © 2012 by the Congress of Neurological Surgeons GBP £20.00 Both primary and secondary insults activate the release of cellular mediators including proinflammatory cytokines, prostaglandins, free radicals, and complement.
Since the anaerobic metabolism is inadequate to maintain cellular energy states, the ATP-stores deplete and failure of energy-dependent membrane ion pumps occurs. 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).
It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwideFor full access to this pdf, sign in to an existing account, or purchase an annual subscription. To examine hemispheric differences in cerebral autoregulation in children with traumatic brain injury (TBI). Cerebrovascular pressure reactivity can be monitored by using the pressure reactivity index (PRx), which is based on intracranial pressure monitoring. C. Werner, K. Engelhard, Pathophysiology of traumatic brain injury, The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. Translocation of phosphatidylserine initiates discrete but progressive membrane disintegration along with lysis of nuclear membranes, chromatine condensation, and DNA-fragmentation. cerebrovascular constriction or dilation in response to increases or decreases in CPP) is impaired or abolished in most patients.Compared with CBF autoregulation, cerebrovascular COPost-traumatic cerebral vasospasm is an important secondary insult that determines ultimate patient outcome.Cerebral metabolism (as reflected by cerebral oxygen and glucose consumption) and cerebral energy state (as reflected by tissue concentrations of phosphocreatine and ATP or indirectly by the lactate/pyruvate ratio) are frequently reduced after TBI and present with considerable temporal and spatial heterogeneity.As an alternative pathophysiological event, hypermetabolism of glucose may occur.TBI is characterized by an imbalance between cerebral oxygen delivery and cerebral oxygen consumption. However, apoptosis becomes evident hours or days after the primary insult.
Yet, the unpredictability of the individual's pathophysiology requires monitoring of the injured brain in order to tailor the treatment according to the specific status of the patient.Oxford University Press is a department of the University of Oxford. It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. superoxide dismutase, glutathione peroxidase, and catalase) induces peroxidation of cellular and vascular structures, protein oxidation, cleavage of DNA, and inhibition of the mitochondrial electron transport chain.Oedema formation frequently occurs after TBI. 1–4 In the acutely injured brain, cerebral autoregulation may be dysfunctional, leading to episodes of hypoperfusion or hyperemia. Search for other works by this author on: Listing a study does not mean it has been evaluated by the U.S. Federal Government.
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