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  • hypoxia
  • High altitude cerebral edema (HACE) is a severe and sometimes fatal form of altitude sickness that results from capillary fluid leakage due to the effects of hypoxia on the mitochondria -rich endothelial cells of the blood-brain barrier. (wikipedia.org)
  • develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia, sodium depletion, and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. (studystack.com)
  • 1-6 Such increased lipolytic activity has mainly been studied by measuring free fatty acids and membrane phospholipids extracted from brain homogenate samples in animal models of ischaemia, hypoxia, hypoglycaemia, and epilepsy. (bmj.com)
  • occurs
  • If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centres in the pons and medulla oblongata . (wikipedia.org)
  • Vasogenic edema occurs due to a breakdown of the tight endothelial junctions that make up the blood-brain barrier. (wikipedia.org)
  • Herniation occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a one of lesser pressure. (studystack.com)
  • CONCLUSIONS This study suggests that membrane phospholipid degradation occurs in human cerebral ischaemia. (bmj.com)
  • Cerebral edema typically occurs after several hours of treatment with insulin and intravenous fluids but can also occur at the time of presentation of DKA before treatment is started. (neurologyadvisor.com)
  • Although severe, clinically apparent cerebral edema occurs in just 1% of DKA episodes in children, numerous studies have demonstrated that mild cerebral edema, associated with only minimal or no alterations in mental status, is present in the majority of children during DKA treatment. (neurologyadvisor.com)
  • DKA-related cerebral edema occurs most commonly after several hours of DKA treatment with insulin and intravenous fluids, but can also occur at the time of presentation to the emergency department, before treatment is administered. (neurologyadvisor.com)
  • Epidemiologic studies demonstrate that DKA-related cerebral edema occurs most frequently in children with severe acidosis and severe hypocapnia as well as marked dehydration (high blood urea nitrogen concentrations In addition, a lesser rise in measured serum sodium concentration during DKA treatment as the serum glucose concentration falls has been identified as associated with greater risk for DKA-related cerebral edema. (neurologyadvisor.com)
  • Injury
  • The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. (ubc.ca)
  • This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. (ubc.ca)
  • Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. (ubc.ca)
  • REVIEW Open AccessClinical pathophysiology of hypoxicischemic brain injury after cardiac arrest:a "two-hit" modelMypinder S. Sekhon1,2*, Philip N. Ainslie2 and Donald E. Griesdale1,3,4AbstractHypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologicdisability in survivors. (ubc.ca)
  • Among factors that may be implicated in this secondary injury includereperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia,fluctuations in arterial carbon dioxide, and concomitant anemia.Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research toidentify therapeutic targets. (ubc.ca)
  • and the extremely fast scale associated with traumatic brain injury. (springer.com)
  • Intracranial hypertension is the largest cause of death in young patients with severe traumatic brain injury 1) . (neurocirugia.com)
  • The management of traumatic brain injury progressed significantly in the 1980s and 1990s due to advances in neuroimaging (widespread introduction of CT scanning), prehospital management, neurointensive care (widespread adoption of ICP monitoring and tiered therapeutic protocols) and rehabilitation. (neurocirugia.com)
  • Both proteins are considered specific markers of brain damage after stroke, 1 2 3 4 5 traumatic brain injury, 6 7 8 cardiac surgery under cardiopulmonary bypass condition, 9 10 or cardiac arrest. (ahajournals.org)
  • A variety of experimental findings suggest both a detrimental (induction of neuronal cell death 19 ) and a beneficial (induction of reactive synaptogenesis and plasticity processes 20 ) potential of protein S-100B dependent on concentration and time elapsed since brain injury. (ahajournals.org)
  • seizures
  • Glycerol is an end product of membrane phospholipid degradation and has been used to study membrane phospholipid degradation in brain homogenates after cerebral ischaemia and seizures. (bmj.com)
  • The most common symptoms of DKA-related cerebral edema include mental status changes (confusion, irritability, obtundation) associated with severe headache, recurrence of vomiting, seizures, hypertension, inappropriate slowing of heart rate, and/or signs of increased intracranial pressure. (neurologyadvisor.com)
  • glial
  • It can occur in neurons, glial cells, axons (axonal swelling) and myelin sheaths (intramyelinic edema). (mussenhealth.us)
  • Consequently, there was a demand for neurobiochemical markers highly specific for astroglial brain tissue, and glial fibrillary acidic protein (GFAP) was considered a high-priority candidate. (ahajournals.org)
  • oxygen
  • During an ischemic stroke , a lack of oxygen and glucose leads to a breakdown of the sodium-calcium pumps on brain cell membranes, which in turn results in a massive buildup of sodium and calcium intracellularly. (wikipedia.org)
  • tissue
  • Recent findings have directly linked major brain development, mechanisms, and diseases to the mechanical response of the brain both at the cellular and tissue levels. (springer.com)
  • An increase in volume (in brain tissue, blood, or CSF) does not increase the ICP. (studystack.com)
  • Protein S-100B, however, is expressed not only in brain tissue but also in a variety of other cell types, under both physiological and pathological conditions. (ahajournals.org)
  • occur
  • Brain- none CSF- redistributed into compliant paraspinal CSF space Blood- venous blood forced into internal jugular veins When compensatory mechanisms are exhausted, ICP rises more rapidly Eventually, the compensatory mechanisms are exhausted and a sharp rise in ICP will occur. (slideplayer.com)
  • When does diabetic ketoacidosis-related cerebral edema typically occur? (neurologyadvisor.com)
  • Fig. 2) AVMs occur anywhere in the brain or spinal cord, but the majority are supratentorial. (jaocr.org)
  • mannitol
  • The long-term beneficial effects of mannitol are still controversial, and there is some evidence that repeated doses of mannitol may even aggravate brain edema. (ahajournals.org)
  • fluid
  • Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain . (wikipedia.org)
  • In the first part of this manuscript, we present the current understanding of the fundamental mechanics of the brain by reviewing its solid, fluid, electrochemical, and electromechanical components. (springer.com)
  • It is the accumulation of excess fluid within the brain parenchyma. (brainscape.com)
  • however, there are no clear associations between the use of particular fluid treatment protocols and increased risk of DKA-related cerebral edema. (neurologyadvisor.com)
  • extracellular space
  • The increase in extracellular space osmolarity will result in a marked increase in extracellular water, i.e. vasogenic edema (hematoxylin-eosin stain, original magnification x200). (mussenhealth.us)
  • Pathological specimens of vasogenic edema show leakage of plasma from the vessel and diffuse expansion of the extracellular space in the white matter (Fig. 4.15). (mussenhealth.us)
  • apparent
  • This apparent lack of interest from both the brain and mechanics communities is also in clear distinction with other major organs such as the heart, arteries, lungs, or bones for which there exist well-established theories and large scientific communities. (springer.com)
  • hyperintensity
  • a T2-weighted image shows central necrosis as slightly hyperintense (arrow) and peripheral vasogenic edema as very hyperintense in the left hemisphere (arrowheads).Multiple lesions of toxoplasmosis are also seen in the right occipital and left periventricular areas.b DW image reveals vasogenic edema as hypointense, while the central necrosis shows hyperintensity on DW image. (mussenhealth.us)
  • In some cases, T2 hyperintensity is identified in the adjacent brain parenchyma consistent with areas of gliosis. (jaocr.org)
  • blood
  • An increase in the volume of any of the contents within the intracranial vault must be met with a decrease in the volume of another or the intracranial pressure will increase V (vault)= V (CSF) + V (brain) + V (blood) + V (other) First described over 200 years ago. (slideplayer.com)
  • 1 Over the past few years, the use of previously recommended therapies such as barbiturates or hyperventilation has been increasingly questioned since it was recognized that they may critically reduce the CPP through negative effects on the systemic blood pressure or excessive cerebral vasoconstriction with secondary ischemic damage. (ahajournals.org)
  • Combined treatment yields no additional benefit compared with single treatment, probably because of early blood-brain barrier breakdown. (ahajournals.org)
  • The femoral artery and vein were catheterized to monitor blood pressure and blood gases and to administer contrast agent. (ahajournals.org)
  • the pressure needed to ensure blood flow to the brain. (studystack.com)
  • Smaller lesions may be difficult to visualize on non-contrast CT since they are filled with flowing blood that is isoattenuating to slightly hyperattenuating to normal brain. (jaocr.org)
  • patients
  • GFAP was found to be a more sensitive marker of brain damage in patients with smaller lacunar lesions or minor strokes. (ahajournals.org)
  • cellular
  • Cytotoxic or cellular edema is hyperintense on DW images and associated with decreased ADC. (mussenhealth.us)
  • Further, most brain pathologies depend on many different factors and their physical manifestation may be conveniently ignored by focusing on genetics and cellular function as the primary driver. (springer.com)
  • parenchyma
  • The classic AVM (also known as pial AVM) results from an abnormal connection between the arteries that normally supply the brain parenchyma and the veins that would normally drain this region. (jaocr.org)
  • barrier
  • the result of rupture of the CSF brain barrier and is usually a result of obstructive or uncontrolled hydrocephalus. (studystack.com)