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Edema (darker areas) surrounding a secondary brain tumor.
Cerebral edema or cerebral œdema is an excess accumulation of fluid in the intracellular or extracellular spaces of the brain.
Trauma or injury can cause the rupture of cerebral blood vessels, which changes the water, sodium, and potassium levels inside the brain. Water and sodium levels continue to rise in the first several days after injury, and regional cerebral ischemia can occur.
Symptoms include nausea, vomiting, blurred vision, faintness. If herniation occurs, respiratory symptoms such as respiratory arrest can also occur due to compression of the respiratory center.
Recently, many studies on the mechanical properties of the brain edema have been conducted. Most are based on the technique of Finite Element Analysis (FEA), which is a widely-used numerical method in solid mechanics. For example, Gao and Ang used the FEA method to study changes in intracranial pressure during craniotomy operations. The model corresponds well to clinical data. There are multiple advantages to using FEA. First, the cost of the numerical procedure is much less than that of cadaver experiments. Second, parameters can easily be modified using the computer model. Third, the numerical results can be useful in achieving insight and understanding of the disease process. However, due to the complicated theories of the nonlinear mechanics, some aspects of FEA, such as the constitutive equations and meshing process, still need to be improved to facilitate its use in research.
Vasogenic edema occurs due to a breakdown of the tight endothelial junctions which make up the blood–brain barrier (BBB). This allows intravascular proteins and fluid to penetrate into the parenchymal extracellular space. Once plasma constituents cross the BBB, the edema spreads; this may be quite rapid and extensive. As water enters white matter it moves extracellularly along fiber tracts and can also affect the gray matter. This type of edema may result from trauma, tumors, focal inflammation, late stages of cerebral ischemia and hypertensive encephalopathy.
Mechanisms contributing to BBB dysfunction include physical disruption by arterial hypertension or trauma, and tumor-facilitated release of vasoactive and endothelial destructive compounds (e.g. arachidonic acid, excitatory neurotransmitters, eicosanoids, bradykinin, histamine, and free radicals). Subtypes of vasogenic edema include:
- Hydrostatic cerebral edema
- This form of cerebral edema is seen in acute, malignant hypertension. It is thought to result from direct transmission of pressure to cerebral capillaries with transudation of fluid from the capillaries into the extravascular compartment.
- Cerebral edema from brain cancer
- Cancerous glial cells (glioma) of the brain can increase secretion of vascular endothelial growth factor (VEGF), which weakens the junctions of the blood–brain barrier. Dexamethasone can be of benefit in reducing VEGF secretion.
- High altitude cerebral edema
- High altitude cerebral edema (or HACE) is a severe and sometimes fatal form of altitude sickness. HACE results from capillary fluid leakage due to the effects of hypoxia on the mitochondria-rich endothelial cells of the blood–brain barrier.
- Symptoms can include headache, loss of coordination (ataxia), weakness, disorientation, memory loss, psychotic symptoms (hallucinations and delusions), and coma. HACE generally occurs after a week or more at high altitude. If not treated quickly, severe cases can result in death. Immediate descent by 2,000 - 4,000 feet is a crucial life-saving measure. Medications such as dexamethasone can be prescribed for treatment in the field, but proper training in their use is required. Anyone suffering from HACE should be evacuated to a medical facility for proper follow-up treatment. A Gamow bag can sometimes be used to stabilize the sufferer before transport or descending.
- Climbers may also suffer high altitude pulmonary edema (HAPE), which affects the lungs. While not as life threatening as HACE in the initial stages, failure to descend to lower altitudes or receive medical treatment can also lead to death.
In cytotoxic edema, the BBB remains intact. It occurs due to a disruption in cellular metabolism that impairs functioning of the sodium and potassium pump in the glial cell membrane, leading to cellular retention of sodium and water. Swollen astrocytes occur in gray and white matter. Cytotoxic edema is seen with various toxins, including dinitrophenol, triethyltin, hexachlorophene, and isoniazid. It can occur in Reye's syndrome, severe hypothermia, early ischemia, encephalopathy, early stroke or hypoxia, cardiac arrest, and pseudotumor cerebri.
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 build up of sodium and calcium intracellularly. This causes a rapid uptake of water and subsequent swelling of the cells. It is this swelling of the individual cells of the brain that is seen as the main distinguishing characteristic of cytotoxic edema, as opposed to vasogenic wherein the influx of fluid is typically seen in the interstitial space rather than within the cells themselves. While not all patients who have experienced a stroke will develop a severe edema, those who do have a very poor prognosis.
In most instances, cytotoxic and vasogenic edema occur together. It is generally accepted that cytotoxic edema is dominant immediately following an injury or infarct, but gives way to a vasogenic edema that can persist for several days or longer. The use of specific MRI techniques has allowed for some differentiation between the two mechanisms and suggests that in the case of trauma, the cytotoxic response dominates 
Normally, the osmolality of cerebral-spinal fluid (CSF) and extracellular fluid (ECF) in the brain is slightly lower than that of plasma. Plasma can be diluted by several mechanisms, including excessive water intake (or hyponatremia), syndrome of inappropriate antidiuretic hormone secretion (SIADH), hemodialysis, or rapid reduction of blood glucose in hyperosmolar hyperglycemic state (HHS), formerly hyperosmolar non-ketotic acidosis (HONK). Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared to the serum. This creates an abnormal pressure gradient and movement of water into the brain, causing edema.
Interstitial edema occurs in obstructive hydrocephalus due to a rupture of the CSF-brain barrier. This results in trans-ependymal flow of CSF, causing CSF to penetrate the brain and spread to the extracellular spaces and the white matter. Interstitial cerebral edema differs from vasogenic edema as CSF contains almost no protein.
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- MedPix Vasogenic Edema