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Pathophysiology of brain edema formation. Guohua Xi, MD, Richard F. Keep, PhD, Julian T. Hoff, MD*. Department of Neurosurgery, University of Michigan, MC. Traumatic brain edema is a secondary phenomenon of traumatic brain injury. It manifests during a time interval by escape of fluid from the vascular compartment. By definition cerebral edema is the excess accumulation of water in the intra-and/or extracellular spaces of the brain [1]. Pathophysiology of cerebral edema at cellular level is complex. Damaged cells swell, injured blood vessels leak and blocked absorption pathways force fluid to enter brain tissues.


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This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema.

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Astrocytes, brain edema, capillaries, cerebrospinal fluid, endothelium Introduction Historically, the goal cerebral edema pathophysiology brain protection following injury has been to reduce neuronal damage.

Edema, the inevitable accompaniment, was considered a secondary event.


A renewed interest in edema, its molecular antecedents and its importance in all but the smallest ischemic insults has shifted this paradigm. Hydrostatic cerebral edema This form of cerebral edema cerebral edema pathophysiology seen in acute malignant hypertension.

Cerebral edema - Wikipedia

It cerebral edema pathophysiology 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 cerebral edema pathophysiology glioma of the brain can increase secretion of vascular endothelial growth factor VEGFwhich weakens the junctions of the blood—brain barrier.

Dexamethasone can be of benefit in reducing VEGF secretion.

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HACE generally occurs after a week or more at cerebral edema pathophysiology altitude. If not treated quickly, severe cases can result in death. The disruption of the cerebral capillary provides the underlying mechanism for vasogenic edema. The amount of edema is greatest in the white matter increased water and sodium in the extracellular spaces, decreased potassium ; but the same changes may take place in grey matter but less so.

Molecular pathophysiology of cerebral edema

The astrocytes become swollen. Normally, there are cerebral edema pathophysiology types of vasopressin receptors present cerebral edema pathophysiology the body. V1A receptors are present in smooth muscle of vessels while V1B is present in anterior pituitary.

V2 receptors are primarily located in renal collecting ducts. It promotes free water reabsorption through cyclic adenosine monophosphate pathway.

Cerebral edema

In various trials, it was found that conivaptan was effective in treating patients with euvolaemic or hypervolaemic hyponatraemia and raise serum sodium level by 6. Matrix metalloproteinase inhibitors In various rodent models, during vasogenic oedema, matrix metalloproteinase MMP inhibitors were used and it cerebral edema pathophysiology found that they restore BBB integrity in early phase, but not after 48 h.


But, they have major drawback that they delayed recovery due to their role in angiogenesis and neurogenesis. Received Mar 13; Accepted Apr This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license http: This article has been cited by other cerebral edema pathophysiology in PMC.

Abstract Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head cerebral edema pathophysiology. In the edematous brain, excess accumulation of extracellular fluid results in elevation of intracranial pressure, leading to impaired nerve function.

Despite the seriousness of brain edema, only symptomatic treatments to remove edema fluid are currently available.