Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2008
Microglial activation and brain injury after intracerebral hemorrhage.
Microglial activation and thrombin formation contribute to brain injury after intracerebral hemorrhage (ICH). Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) are 2 major proinflammatory cytokines. In this study, we investigated whether thrombin stimulates TNF-alpha and IL-1beta secretion in vitro, and whether microglial inhibition reduces ICH-induced brain injury in vivo. ⋯ Tuftsin reduced thrombin-induced upregulation of TNF-alpha and IL-1beta. In vivo, microglia were activated after ICH, and intracerebral injection of tuftsin reduced brain edema in the ipsilateral basal ganglia (81.1 +/- 0.7% vs. 82.7 +/- 1.3% in vehicle-treated group; p < 0.05) after ICH. These results suggest a critical role of microglia activation in ICH-related brain injury.
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Acta Neurochir. Suppl. · Jan 2008
Predictive values of age and the Glasgow Coma Scale in traumatic brain injury patients treated with decompressive craniectomy.
The use of decompressive craniectomy (DC) as an aggressive therapy for traumatic brain injury (TBI) has gained renewed interest. While age and the Glasgow Coma Scale (GCS) are frequently correlated with outcome in TBI, their prognostic values after decompressive craniectomy are ill-defined. ⋯ This data suggests that in TBI patients treated with DC, age correlates with outcome while the correlation between GCS and outcome is age-dependent.
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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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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.