Acta neurochirurgica. Supplement
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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
Long-term effects of melatonin after intracerebral hemorrhage in rats.
Free radical scavengers have been shown to improve short-term outcome after intracerebral hemorrhage (ICH). The purpose of this study was to evaluate whether melatonin (a potent free radical scavenger and an indirect antioxidant) can improve short- and/or long-term neurological function after ICH, which was induced by collagenase injection into the striatum of adult rats. ⋯ Neurological and behavioral testing was performed at several time points from 1 day to 8 weeks post-ICH. Neurological and behavioral deficits were observed in ICH rats at all time points, but the melatonin treatment regimen did not improve performance or level of brain injury.
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Acta Neurochir. Suppl. · Jan 2008
Biomechanical modeling of decompressive craniectomy in traumatic brain injury.
Decompressive craniectomy is the final phase in the graded scheme of critical care management of refractory raised intracranial pressure following severe traumatic brain injury. We aim to define the optimal size for decompressive craniectomy so that a good balance is achieved between reduction of raised ICP and the extent of trans-calvarial herniation. Provision of such quantitative data will also allow for improved data comparison in clinical trials addressing the surgical management of severe head injury. ⋯ Finite element mesh modeling in the scenario of reafractory raised intracranial pressure following severe head injury may be able to guide the optimal conduct of decompressive surgery so as to effect a reduction in intracranial pressure whilst minimizing trans-calvarial brain herniation.
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Acta Neurochir. Suppl. · Jan 2008
The antioxidant effects of melatonin after intracerebral hemorrhage in rats.
Free radical mechanisms are involved in secondary brain injury after intracerebral hemorrhage (ICH). Since melatonin is a potent free radical scavenger and indirect antioxidant, the objective of this study was to evaluate whether melatonin administration would attenuate oxidative stress, brain edema, and neurological deficits in a rat model of ICH. Animals were assigned into groups consisting of sham (needle trauma), vehicle, and melatonin (15 or 150 mg/kg). ⋯ Results demonstrated dramatically increased lipid peroxidation after collagenase-induced ICH; however, melatonin treatment effectively attenuated this lipid peroxidation. Nonetheless, neurological scoring and brain water content in the right basal ganglia was without significant difference between any treatment regimens (15 or 150 mg/kg of melatonin) or time points of drug administration (15 min or 3 h post-ICH). Therefore, melatonin reduced oxidative stress but did not change extent of brain edema or neurologic deficits.