Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
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We investigated the neuroprotective effects of pre- and postconditioning on infarct volume in the transient middle cerebral artery occlusion (MCAo) model in rats. Thirty-two male rats were divided into occlusion, preconditioning, postconditioning and both pre- and postconditioning groups. MCAo (120 minutes) was monitored with continuous cerebral tissue oxygen (O2) pressure (PtiO2). ⋯ Comparison of infarct volumes showed a significant difference between the conditioned groups and occlusion group. Although there was better protection in the preconditioning group compared with the other two conditioned groups, the results did not reach statistically significant levels. The results suggest that preconditioning, postconditioning and pre/post conditioning have protective effects on cerebral ischemia.
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Clinical Trial
Outcomes and cost-effectiveness of gamma knife radiosurgery and whole brain radiotherapy for multiple metastatic brain tumors.
We aimed to analyze the outcomes and cost-effectiveness of gamma knife radiosurgery (GKRS) and whole brain radiotherapy (WBRT) for multiple metastatic brain tumors. Over a period of 5 years, 156 patients with multiple metastatic brain tumors were enrolled and freely assigned by the referring doctors to either gamma knife radiosurgery (GKRS, Group A, n=56), or to whole brain radiotherapy (WBRT, Group B, n=100). The follow-up time was set at 1200 days (3.3 years) post-treatment. ⋯ The cost-effectiveness per KPS score was also higher for the GKRS treatment (US$139/KPS score) than for WBRT (US$229/KPS score), p<0.01. Thus, the mortality rate for multiple metastatic brain tumors treated by GKRS is significantly better with a good initial KPS score and when the tumor number is 2-5. GKRS results in a better post-treatment KPS score, QALY, and higher cost-effectiveness than WBRT for treating multiple metastatic brain tumors.
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The neuroprotective effect of N-acetylcysteine (NAC), a sulfhydryl-containing antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) in rats was assessed. NAC was administered to rats after the induction of SAH. Neurological deficits and brain edema were investigated. ⋯ We found that NAC markedly reversed the SAH-induced neurological deficit and brain edema. We further investigated the mechanism involved in the neuroprotective effects of NAC on rat brain tissue and found that NAC significantly increased CuZn-SOD and GSH-Px activity and decreased MDA content in the SAH brain. NAC has the potential to be a novel therapeutic strategy for the treatment of SAH, and its neuroprotective effect may be partly mediated via enhancing the activity of endogenous antioxidant enzymes and inhibiting free radical generation.
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We aimed to develop a double-injection model of intracerebral hemorrhage (ICH) in rabbits and to evaluate it as a tool for investigating post-ICH brain injury. Rabbits were injected with 300microL fresh autologous whole blood into the right basal ganglia. ⋯ At 1, 3 and 7 days after ICH, there were significant differences in the total neurological scores (p<0.01) and BWC (p<0.01) between a sham-operated group and the ICH group. These findings suggest that the model produces a persistent neurological deficit, hematoma volume and perihematomal edema and closely mimics human hypertensive basal ganglia ICH; it is a controllable and reproducible hematoma that lends itself to quantitative investigation.
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Erythropoietin (Epo) has neuroprotective activity in a variety of settings. Thus, we investigated whether Epo has a role in the functional recovery of rats after facial nerve injury. The right facial nerve of 24 Wistar rats (6 wks old) was crushed twice at the level of the stylomastoid foramen, for 30 s each time, using jeweler's forceps held perpendicular to the nerve. ⋯ There was no significant difference between low dose Epo-treated rats (1,000 U/kg body weight) and the placebo-treated rats. These results suggest that high dose Epo can promote the functional recovery of rats following facial nerve injury. Further studies are warranted to probe alternative treatment schedules (dose, mode of administration), underlying histological mechanisms and combination treatment with additional neuroprotective factors.