Acta neurochirurgica. Supplement
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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
Modulation of AQP4 expression by the selective V1a receptor antagonist, SR49059, decreases trauma-induced brain edema.
Currently, there are no pharmacological treatments available for traumatically induced brain edema and the subsequent rise of ICP. Evidence indicates that Aquaporin-4 (AQP4) plays a significant role in the pathophysiology of brain edema. Previously we have reported that SR49059 reduced brain edema secondary to ischemia. We, therefore, examined whether the selective V1a receptor antagonist, SR49059, reduces brain edema by modulating AQP4 expression following cortical contusion injury (CCI). ⋯ SR49059 significantly reduced trauma-induced AQP4 up-regulation in the contused hemisphere. Moreover, brain water content was also significantly reduced paralleling the AQP4 suppression. These data provide further support that vasopressin (AVP) and V1a receptors can control water flux through astrocytic plasma membranes by regulating AQP4 expression. Taken in concert, these results affirm our laboratories contention that AQP4 can be effectively modulated pharmacologically.
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Approximately 15% of all strokes are due to intracerebral hemorrhage, and of these, 5 to 9% will occur in the pons, with mortality approximately 60% of the time. However, there is not an adequate animal model to fully address this important clinical problem. To this end, pontine hemorrhage was induced in rats using stereotaxic injection of 0.15 units of collagenase. ⋯ All tested parameters were significantly increased, compared to sham, without any differences between time points. Furthermore, the extent of brainstem edema was highly correlated with neurological score, inclined plane, and body temperature. This new pontine hemorrhage rat model demonstrated brain edema and neurological deficits, and can be used to test treatment strategies for pontine hemorrhage.
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Acta Neurochir. Suppl. · Jan 2008
Effect of amantadine sulphate on intracerebral hemorrhage-induced brain injury in rats.
Recent studies have shown that amantadine, an uncompetitive N-methyl-d-aspartate receptor antagonist and dopamine agonist, is effective for the treatment of various cerebral disorders and causes relatively mild side effects. In this study, we investigated whether administration of amantadine will provide a neuroprotective effect in the intracerebral hemorrhage (ICH) rat model. A total of 15 male Sprague Dawley rats (300-380 g) were divided into sham, ICH-untreated, and ICH-treated with amantadine sulphate groups. ⋯ Our data demonstrates that ICH caused significant neurological deficit associated with marked brain edema. Amantadine did not reduce brain injury after ICH; neurological function and brain edema in the treated group were not different from those of the untreated group. We conclude that amantadine sulphate does not offer neuroprotection in acute stage of experimental ICH-induced brain injury.