Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2008
The relationship between intracranial pressure and brain oxygenation following traumatic brain injury in sheep.
While it is understood that raised intracranial pressure (ICP) after traumatic brain injury (TBI) may negatively impact on brain tissue oxygenation (PbtO2), few studies have characterized the inter-relationship between these two variables, particularly in a large animal model that replicates the human gyrencephalic brain. The current study uses an ovine model to examine the dynamics of ICP and PbtO2 after TBI. ⋯ Our results suggest that TBI results in early changes in ICP that are associated with profound declines in PbtO2, and may indicate the need for earlier management of ICP after TBI.
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Acta Neurochir. Suppl. · Jan 2008
Changes in brain biochemistry and oxygenation in the zone surrounding primary intracerebral hemorrhage.
While the management of primary intracerebral hemorrhage (ICH) remains controversial, there remains a subset of patients that undergo clot evacuation. This study aims to characterize brain physiology and biochemistry after surgery for this condition. ⋯ In spontaneous ICH, derangements in the perilesional tissue demonstrated by local techniques of PbO2 monitoring and CMD are not seen in global indices such as the PRx.
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Acta Neurochir. Suppl. · Jan 2008
The modulation of aquaporin-4 by using PKC-activator (phorbol myristate acetate) and V1a receptor antagonist (SR49059) following middle cerebral artery occlusion/reperfusion in the rat.
We have pursued the concept that traumatic brain edema is predominantly cellular and that water entry is modulated in part by aquaporins. Aquaporin-4 (AQP4) has been shown to play a significant role in cellular edema formation. Phorbol myristate acetate (PMA) is a potent PKC activator; purportedly involved in modulation of AQP4 activity. Alternatively, AQP4 may be regulated by arginine-vasopressin. Administration of the vasopressin antagonist (SR49059) reduced brain water content and sodium shift following MCAo. To investigate if edema formation is affected by the reduction of AQP4 expression, we utilized PMA and SR49059 following middle cerebral artery occlusion model (MCAo), and measured AQP4 expression by Western-Blot (WB) techniques. ⋯ These studies support the hypotheses that PMA and SR49059 may be useful in reducing cerebral water accumulation by modulating AQP4 expression and that pharmacological manipulation of AQP4 may emerge as a viable strategy for the reduction of fulminating edema following ischemic injury.
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Acta Neurochir. Suppl. · Jan 2008
Patient and aneurysm characteristics in multiple intracranial aneurysms.
Multiple aneurysms occur in up to one-third of people with intracranial aneurysms. Of such patients, epidemiological data, clinical information, and aneurysm characteristics (of both unruptured and ruptured aneurysms in the same patients) were gathered in this retrospective review. ⋯ Ruptured aneurysms were significantly larger than unruptured ones. Although discussed controversially, most of our population's ruptured aneurysms were 10mm or smaller in size. Considering this, our study may contribute to improve the management of patients with intracranial aneurysms.
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Acta Neurochir. Suppl. · Jan 2008
Deficiency of CD18 gene reduces brain edema in experimental intracerebral hemorrhage in mice.
Experimental studies of intracerebral hemorrhage (ICH) point toward leukocytes as a major contributor to ICH-induced brain injury. Leukocyte and endothelial cell adhesion molecules are responsible for injurious neutrophil-endothelial cell interactions in vasculature. Since deficiency of leukocyte-expressed CD18 protects against ischemia-reperfusion injury, we hypothesized that such deficiency may have similar effect in ICH-induced injury. ⋯ Our study showed that the increase in brain water content caused by ICH was significantly smaller in CD18 knockout mice compared with wild-type mice (p < 0.05, Student t-test). This result correlated with a tendency toward improvement of neurological function and a decrease in mortality. We conclude that CD18 deficiency significantly reduces brain edema after ICH, which corresponds with a trend toward reduction in neurological deficit and mortality.