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Possible Relationship between Vascular Permeability Factors, Endothelial Cells, and Peritumoral Brain Edema

A Neurosurgeon’s Perspective

  • Chapter
Endothelial Cell Dysfunctions

Abstract

Cerebral edema is a significant cause of the neurological morbidity associated with malignant brain tumors. Patients afflicted with intracranial neoplasms typically present with progressively worsening headaches, vomiting, blurred vision, double vision, and depressed level of consciousness. All of these clinical features are clearly related to elevated intracranial pressure (ICP), which may rapidly result in a patient’s demise if not treated promptly and effectively. The brain edema associated with cerebral tumors is an ultrafiltrate of plasma containing water, electrolytes, and plasma proteins, that emanates from the brain tumor microvasculature. Edema fluid typically infiltrates the white matter surrounding an intracerebral tumor in a diffuse manner, while relatively sparing the adjacent cortex. This excessive accumulation of cerebral interstitial tissue fluid contributes to the distortion of normal intracranial structures, and to elevation of the ICE As a result, cerebral edema is frequently as culpable for a brain tumor patient’s symptoms as the primary intracerebral neoplasm. It is now widely accepted that this excessive fluid accumulation results from a flaw in the integrity of the blood-brain barrier. The blood-brain barrier is both an anatomical and a physiological system which normally regulates the entry and egress of substances between the cerebral interstitial and intravascular compartments. The functional components of the blood-brain barrier occur primarily at the level of the vascular endothelial cell and, to a lesser extent, the basement membrane and astrocytic processes which invest the cerebral microvasculature.

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Criscuolo, G.R. (1992). Possible Relationship between Vascular Permeability Factors, Endothelial Cells, and Peritumoral Brain Edema. In: Simionescu, N., Simionescu, M. (eds) Endothelial Cell Dysfunctions. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0721-9_28

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