Abstract
The brain is enclosed in an unyielding container. Any process that causes expansion of one intracranial component necessarily causes compression of the other components. When there is rapid expansion of an intracranial space-occupying lesion, for example edema in the area of injured brain parenchyma, cerebrospinal fluid and venous blood are displaced from the intracranial compartment and the brain is distorted. Ultimately intracranial pressure rises and, when it exceeds the arterial perfusion pressure, blood flow to the brain is impaired. Thereafter neurons die and the opportunity for functional recovery is lost. Because we are currently incapable of resurrecting neurons which die during the initial ischemic or traumatic insult, we must concentrate our therapeutic efforts on the prevention of secondary neuronal injury. This is most often the consequence of brain swelling due to edema and in order to control brain swelling it is imperative that we understand the pathophysiology of brain edema.
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Del Bigio, M.R. (1993). Morphology of Astroglial Swelling in Culture and in the Edematous Brain: An Adaptive Response to a Disturbed Microenvironment. In: Fedoroff, S., Juurlink, B.H.J., Doucette, R. (eds) Biology and Pathology of Astrocyte-Neuron Interactions. Altschul Symposia Series, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9486-1_31
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