Summary
The non-hemorrhagic mass effect of cerebral contusions is commonly attributed to vasogenic edema and/or cytotoxic edema (cellular swelling). We propose that a marked increase in osmolality within the contusion necrosis proper, in which the cellular elements uniformly undergo shrinkage, disintegration and homogenation, represents an important and unique mechanism underlying the contusion edema. The present study demonstrates in a rat model of cerebral contusion, that 1) the osmolality of the contused brain tissue increases rapidly, 2) the increase in osmolality is not caused by changes in inorganic ion contents, suggesting a metabolic production of osmoles or release of idiogenic osmoles, and 3) the contused brain tissue strongly attracts water, provided that blood supply is maintained. We suggest that the primary driving force of water accumulation into contused brain tissue is the elevated colloid osmotic potential of contusion necrosis.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Alexander MJ, Martin NA, Khanna M, Caron M, Becker DP (1994) Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema. Acta Neurochir (Wien) [Suppl] 60: 479–481
Bullock R, Statham J, Patterson D, Wyper D, Hadley D, Teasdale E (1990) The time course of vasogenic oedema after focal human head injury: Evidence from SPECT mapping of blood brain barrier defects. Acta Neurochir (Wien) [Suppl] 51: 286–288
Eriskat J, Schurer L, Kempski O, Baethmann A (1994) Growth kinetics of a primary brain tissue necrosis from focal lesion. Acta Neurochir (Wien) [Suppl] 60: 425–427
Katayama Y, Tsubokawa T, Miyazaki S, Kawamata T, Yoshino A (1990) Oedema fluid formation within contused brain tissue as a cause of medically uncontrollable elevation of intracranial pressure in head trauma patients Acta Neurochir (Wien) [Suppl] 51: 308–310
Katayama Y, Tsubokawa T, Kinoshita K, Himi K (1992) Intraparenchymal fluid-blood levels in traumatic intracerebral hematomas. Neuroradiology 34: 381–383
Kushi H, Katayama Y, Shibuya T, Tsubokawa T, Kuroha T (1994) Gd-DTPA enhanced magnetic resonance imaging of cerebral contusions. Acta Neurochir (Wien) [Suppl] 60: 472–474
Lang DA, Hadley DM, Teasdale GT, Macpherson P, Teasdale E (1991) Gadolinium DTPA enhanced magnetic resonance imaging in acute head injury. Acta Neurochir (Wien) 109: 5–11
Lindenberg R, Freytag E (1957) Morphology of cortical contusion. Arch Pathol 63: 23–42
Madsen FF (1990) Regional cerebral blood flow after a localized cerebral contusion in pigs. Acta Neurochir (Wien) 105: 150–157
Todd NV, Graham DI (1990) Blood brain barrier damage in traumatic brain contusion. Acta Neurochir (Wien) [Suppl] 51: 296–299
Tornheim PA, Prioleau GR, McLaurin RL (1984) Acute responses to experimental blunt head trauma: Topography of cerebral cortical edema. J Neurosurg 60: 473–480
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1998 Springer-Verlag Wien
About this paper
Cite this paper
Katayama, Y., Mori, T., Maeda, T., Kawamata, T. (1998). Pathogenesis of the Mass Effect of Cerebral Contusions: Rapid Increase in Osmolality within the Contusion Necrosis. In: Marmarou, A., et al. Intracranial Pressure and Neuromonitoring in Brain Injury. Acta Neurochirurgica Supplements, vol 71. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6475-4_84
Download citation
DOI: https://doi.org/10.1007/978-3-7091-6475-4_84
Publisher Name: Springer, Vienna
Print ISBN: 978-3-7091-7331-2
Online ISBN: 978-3-7091-6475-4
eBook Packages: Springer Book Archive