Ischemic cerebral edema

Cerebral ischemia causes not only reversible and then irreversible loss of brain function, but also cerebral edema (Symon et al. 1979 Hossman 1983). Ischemic edema is partly cytotoxic and partly vasogenic. Cytotoxic edema starts early, within minutes of stroke onset, and affects the gray more than the white matter, where damaged cell membranes allow intracellular water to accumulate. Vasogenic edema, which starts rather later, within hours of stroke onset, affects the white matter more, where the damaged blood-brain barrier allows plasma constituents to enter the extracellular space. Ischemic cerebral edema reaches its maximum in two to four days and then subsides over a week or two. 

Suda S, Igarashi H, Aral Y, Andou J, Chishiki T, Katayama Y (2007) Effect of edaravone, a free radical scavenger, on ischemic cerebral edema assessed by magnetic resonance imaging. Neurol Med Chir (Tokyo) 47 197-202... 

Bell BA, Symon L, Branston NM (1985) CBF and time thresholds for the formation of ischemic cerebral edema, and effect of reperfusion in baboons. J Neurosurg 62 31-41. 

Excellent biological arguments exist for a direct impact of fever specifically on neurological outcome. On a local level, fever produces increased levels of excitatory amino acids (e.g., glutamate and dopamine), free radicals, lactic acid, and pyr-uvate. There is an increase in cell depolarizations and BBB breakdown. Enzymatic function is impaired and cytoskeletal stability reduced. These events lead to increased cerebral edema, with a possible reduction in CPP as well as larger volumes of ischemic injury. " ... 

MANAGEMENT OF CEREBRAL EDEMA ASSOCIATED WITH ISCHEMIC STROKE... 

Symon L, Branston NM, Chikovani O (1979). Ischemic brain edema following middle cerebral artery occlusion in baboons relationship between regional cerebral water content and blood flow at 1 to 2 hours. Stroke 10 184-191... 

Simard JM, Chen M, Tarasov KV, Bhatta S, Ivanova S, Melnitchenko L, Tsymbalyuk N, West GA, Gerzanich V (2006) Newly expressed SURl-regulated NC(Ca-ATP) channel mediates cerebral edema after ischemic stroke. Nat Med 12 433-440... 

Mannitol, the most commonly employed osmotic diuretic, is a large polysaccharide molecule. It is often selected for use in the prophylaxis or treatment of oliguric ARF. It is not absorbed from the gastrointestinal tract and, therefore, is only administered i.v. with its elimination dependent on the GFR (within 30 to 60 min with normal renal function). Mannitol is distributed within the plasma and extracellular fluid spaces and produces an increase in the serum osmolality and expansion of the circulating volume. It is not generally used for the treatment of edema because any mannitol retained in the extracellular fluid can promote further edema formation. Furthermore, acute plasma volume expansion may challenge individuals with poor cardiac contractility and can precipitate pulmonary edema. Mannitol is commonly administered for the treatment of cerebral edema consequent to head trauma or to hypoxic-ischemic encephalopathy in neonatal foals. Because mannitol promotes water excretion, hypernatremia is a potential complication in patients that do not have free access to water (Martinez-Maldonado Cordova 1990, Wilcox 1991). 

Cerebral insufficiency refers to describe the people with age-related decline in mental function and decrease blood flow to the brain cause by clogged arteries. Platelet activating factor (PAF) is an inflammatory mediator, plays an important role in allergy, inflammatory processes, coronary, and cerebral vasoconstriction [178]. The production and release of PAF in the brain under various pathological conditions, including oxidant stress-induced ischemic injury [179]. The efficiency of EGb-761 on cerebral circulation and metabolism has been demonstrated in various models of cerebrovascular insufficiency and showed beneficial effect like cerebral edema in rats intoxicated with triethyltin chloride (TET) [180]. Moreover, oral or intravenous administrations EGb decrease cerebral edema development in gerbils [181]. In an animal study [182], EGb-761 and an extract of local ginkgo... 

Histopathological and morphological findings with fatal encephalopathy presented in the form of cerebral edema, endothelial hypertrophy and hyperplasia, and perivascular glial proliferation. Various ischemic disorders were also reported cell necrosis and neuronal loss in isocortex and basal ganglia... 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

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