Abstract
Elevation of intracranial pressure in the clinical and experimental setting can be induced by a variety of brain insults. Cerebrovascular engorgement (swelling), may occur as a loss of autoregulation which would elevate intracranial pressure because of an increased blood volume. An increase of ICP may also result from disturbances at the capillary level by extravasation of serum fluid into the interstitium. Formation of vasogenic brain edema may continue as long as the propelling forces of the arterial pressure maintains an effective transmural pressure gradient (13,14). The area of increased permeability (13,14) and the duration of the opening of the blood-brain barrier (4,14) are additional variables. The increased interstitial fluid could lead to an increased brain volume and, hence, a further rise in intracranial pressure. Brain insults can affect glial and neuronal metabolism so that the cellular function is significantly altered. Examples comprise the processes that occur with ischemia and hypoxia. Blockade of cellular energy metabolism may lead to membrane permeability changes and alterations of the sodium pump. Cellular (cytotoxic) edema and swelling may follow (13). An increased water content in the intracellular compartment of the brain may also lead to an overall increase in brain volume and, hence, of the intracranial pressure.
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© 1986 Plenum Press, New York
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James, H.E., Werner, R., del Bigio, M. (1986). Changes in Brain Edema Movement Following Experimental Brain Insults and Acute Therapy. In: Baethmann, A., Go, K.G., Unterberg, A. (eds) Mechanisms of Secondary Brain Damage. NATO ASI Series, vol 115. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5203-7_13
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DOI: https://doi.org/10.1007/978-1-4684-5203-7_13
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