Acta neurochirurgica. Supplement
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In sepsis the brain is frequently affected although there is no infection of the CNS (septic encephalopathy). One possible cause of septic encephalopathy is failure of the blood-brain barrier. Brain edema has been documented in animal models of sepsis. Aggressive fluid resuscitation in the early course of sepsis improves survival and is standard practice. We hypothesized that aggressive fluid administration will increase intracranial pressure (ICP) and may cause critical reductions in cerebral perfusion pressure (CPP). ⋯ Further research is needed to determine the role of ICP/CPP monitoring in patients with sepsis.
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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.
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Acta Neurochir. Suppl. · Jan 2008
Metabolic disturbance without brain ischemia in traumatic brain injury: a positron emission tomography study.
Cerebral ischemia is believed to be an important mechanism of secondary neuronal injury in traumatic brain injury (TBI). ⋯ We conclude that impaired cerebral blood flow and metabolism in the pericontusional region is observed even in the subacute stage after TBI and is unlikely to cause severe further neuronal damage.