Neurosurgery
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Two main forms of cell death are encountered in biology: apoptosis (i.e., programmed cell death) and necrosis (i.e., accidental cell death). Because necrosis and apoptosis can lead to cell removal, one might intuit that they are both desirable in cancer treatment. However, in the setting of glioblastoma multiforme, a malignant brain tumor for which the presence of necrosis is an important diagnostic feature, clinical studies indicate that as the degree of necrosis advances, the patient's prognosis worsens. Despite the apparent importance of this form of cell death, the mechanism of development of necrosis in glioblastomas remains unelucidated. The purpose of this article is to try to resolve this dilemma by hypothesizing the mechanism of necrosis formation in these tumors. ⋯ A complete understanding of the series of events surrounding necrosis development in glioblastomas that is evidence-based is likely to provide targets for future therapies. On the basis of the potential mechanisms of development of necrosis described in this article, we postulate that effective therapies may have to be directed against the pathways that result in the formation of necrosis.
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Posttraumatic temperature manipulations have been reported to significantly influence the inflammatory response to traumatic brain injury (TBI). The purpose of this study was to determine the temporal and regional profiles of messenger ribonucleic acid (mRNA) expression and protein levels for the proinflammatory cytokine interleukin-1beta (IL-1beta), after moderate or severe TBI. The effects of posttraumatic hypothermia (33 degrees C) or hyperthermia (39.5 degrees C) on these consequences of TBI were then determined. ⋯ Injury severity determines the degree of IL-1beta protein level elevation after TBI. The effects of posttraumatic hypothermia on IL-1beta protein levels (an important mediator of neurodegeneration after TBI) may partly explain the established effects of posttraumatic temperature manipulations on inflammatory processes after TBI.
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The treatment of giant intracranial aneurysms is a challenge because of the limitations and difficulty of direct surgical clipping and endovascular coiling. We describe the indications, surgical technique, and complications of saphenous vein extracranial-to-intracranial bypass grafting followed by acute parent vessel occlusion in the management of these difficult lesions. ⋯ With appropriate attention to surgical technique, a saphenous vein extracranial-to-intracranial bypass followed by acute parent vessel occlusion is a safe and effective method of treating giant intracranial aneurysms. A high rate of graft patency and adequate cerebral blood flow can be achieved. Thrombosis of perforating arteries caused by altered blood flow hemodynamics after parent vessel occlusion may be a continuing source of complications.