Acta neurochirurgica. Supplement
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Acute brain edema formation contributes to brain injury after intracerebral hemorrhage (ICH). It has been reported that hyperbaric oxygen (HBO) is neuroprotective in cerebral ischemia, subarachnoid hemorrhage, and brain trauma. In this study, we investigated the effects of HBO on brain edema following ICH in rats. ⋯ In summary, HBO reduced early perihematomal brain edema and HSP-32 levels in brain. HBO-related brain protection does not occur through reduction in thrombin toxicity because HBO failed to attenuate thrombin-induced brain edema. Our results also indicate that HBO treatment after hematoma lysis for ICH may be harmful, since HBO amplifies iron-induced brain edema.
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Acta Neurochir. Suppl. · Jan 2008
Neurological deficits and brain edema after intracerebral hemorrhage in Mongolian gerbils.
We examined the time course of neurological deficits in gerbils after an intracerebral hemorrhage (ICH) induced by autologous blood infusion and examined its correlation with the severity of perihematomal edema. Mongolian gerbils (n = 15) were subjected to stereotaxic autologous blood infusion (30 or 60 microL) into the left caudate nucleus. Corner-turn and forelimb-placing tests were performed before, and 1 and 3 days after ICH. ⋯ Both neurological deficits and perihematomal edema were significantly greater in animals with 60 microL blood infusion compared to the 30 microL infusion group, and both neurological deficits and edema were also greater at 3 days compared to 1 day after ICH. The severity of neurological deficits paralleled the degree of perihematomal edema. We conclude that the Mongolian gerbil is a suitable model for studies on the behavioral effects of ICH.
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Acta Neurochir. Suppl. · Jan 2008
Clinical TrialIntracranial pressure and cerebral oxygenation changes after decompressive craniectomy in children with severe traumatic brain injury.
There has been a resurgence of interest in decompressive craniectomy for traumatic brain injury (TBI), but the impact of craniectomy on intracranial pressure (ICP) and cerebral oxygenation has not been well described for diffuse injury in children. ⋯ In selected pediatric patients with TBI, craniectomy for diffuse brain swelling can significantly improve ICP and cerebral oxygenation control. The use of the procedure in appropriate settings does not appear to increase the proportion of disabled survivors.
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Acta Neurochir. Suppl. · Jan 2008
Effect of increased intracranial pressure on cerebral vasospasm in SAH.
Increased ICP is common and might precipitate cerebral vasospasm (VSP)-induced ischemic events in aneurysmal SAH (ASAH).Our objective was to determine if there is an association between increased ICP and transcranial colour coded Doppler-angiographic VSP (TCCD-A VSP) in relation to delayed neurological deficit (DND) and poor outcome. ⋯ Increased ICP, not decreased CPP, was related to VSP. The combination of TCCD-A VSP and increased ICP was predictive of poor outcome. Management of acute ASAH should include reduction of increased ICP especially when there is concomitant TCCD-A VSP.
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Acta Neurochir. Suppl. · Jan 2008
ReviewDysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH.
Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation, and chemoregulation. Subarachnoid haemorrhage (SAH) interrupts this regulation of cerebral blood flow. ⋯ CSF ADMA levels are closely associated with the degree and time-course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, the exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme (IPRMT3) or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of preclinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.