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Journal Article

Citation

Bouma GJ, Muizelaar JP, Fatouros P. Acta Neurochir. Suppl. 1998; 71: 272-275.

Affiliation

Medical College of Virgina, Richmond, USA.

Copyright

(Copyright © 1998, Holtzbrinck Springer Nature Publishing Group)

DOI

unavailable

PMID

9779205

Abstract

The pathogenesis of traumatic brain swelling is unclear. Brain edema (increased water content) is considered an important cause of swelling, but there is also evidence that vasodilatation with increased cerebral blood volume (CBV) plays a role. We have evaluated early posttraumatic changes in CBV in 37 head-injured patients, using dynamic contrast-enhanced computerized tomography (CT) in combination with stable Xenon-enhanced CT for measurement of cerebral blood flow (CBF). This technique enables rapid determination of CBV without interfering with patient care. CBV values ranged from 2.0 to 10.1 ml/100 g. There was no relationship the time after injury at which the measurements were taken. CBV did not correlate with CBF in the early posttraumatic period. Patients with raised ICP (> 20 mm Hg) had significantly higher CBV that patients with normal ICP (5.4 +/- 2.1 vs 3.7 +/- 0.9 ml/100 g). Yet, the presence of signs of brain swelling on CT had no relation to the level of CBV. These data suggest that increased CBV may contribute to raised ICP, but that brain swelling is not caused by increased CBV alone, and is more likely accounted for by brain edema. We speculate that cerebral energy failure is the unifying cause of both intracellular edema and cerebral vasodilation leading to swelling of brain tissue.


Language: en

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