Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2006
Clinical TrialOrgan dysfunction assessment score for severe head injury patients during brain hypothermia.
The purpose of this study was to evaluate the utility of a novel organ dysfunction assessment score developed for patients with severe traumatic brain injury during therapeutic brain hypothermia. The Brain Hypothermia Organ Dysfunction Assessment (BHODA) score is calculated through the combined assessment of 6 indices: central nervous system (CNS) function, respiratory function, cardiovascular function, hepatosplanchnic circulation, coagulation, and metabolism. The CNS, hepatosplanchnic circulation, and metabolic indices were based on measurements of cerebral perfusion pressure, gastric tonometry, and blood glucose, respectively. ⋯ A total maximum BHODA score of more than 13 points corresponded to a mortality of 70%. In a multivariate model, the total maximum BHODA score was independently associated with neurological outcome (odds ratio for unfavorable neurological outcome, 2.590: 95% confidence interval, 1.260, 5.327). In conclusion, the BHODA score can help assess multiple organ dysfunction/failure during therapeutic hypothermia and may be useful for predicting outcome.
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Acta Neurochir. Suppl. · Jan 2006
Rapid subthalamic nucleus deep brain stimulation lead placement utilising CT/MRI fusion, microelectrode recording and test stimulation.
Subthalamic nucleus (STN) deep brain stimulation (DBS) has become an established treatment strategy for patients with medically refractory Parkinson's disease (PD). There are however numerous strategies employed for STN lead placement. Variations include method of STN localisation, use of microelectrode recording, number of microelectrode recording passes and time taken for the procedure. ⋯ UPDRS scores, medication use and any surgical complication were assessed. Bilateral STN DBS was an efficacious treatment option for medically refractory PD. We have described a technique which can be performed with effect and low morbidity, and in a time which is well tolerated by patients.
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Acta Neurochir. Suppl. · Jan 2006
Long term results from percutaneous radiofrequency neurotomy on posterior primary ramus in patients with chronic low back pain.
We report on our experience of percutaneous radiofrequency neurotomy (PRN) on the posterior primary ramus (PPR) with at least two years follow-up. ⋯ PRN on the PPR has long-term beneficial effects. Long-term good results can be achieved after proper selection of patients with facet joint related low back pain.
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Acta Neurochir. Suppl. · Jan 2006
Systemic zinc protoporphyrin administration reduces intracerebral hemorrhage-induced brain injury.
Hemoglobin degradation products result in brain injury after intracerebral hemorrhage (ICH). Recent studies found that intracerebral infusion of heme oxygenase inhibitors reduces hemoglobin- and ICH-induced brain edema in rats and pigs. The present study examined whether systemic use of zinc protoporphyrin (ZnPP), a heme oxygenase inhibitor, can attenuate brain edema, behavioral deficits, and brain atrophy following ICH. ⋯ In addition, ZnPP given immediately or 6 hours after ICH improved neurological deficits (p < 0.05). In conclusion, systemic zinc protoporphyrin treatment started at 0 or 6 hours after ICH reduced brain edema, neurological deficits, and brain atrophy after ICH. These results indicate that heme oxygenase may be a new target for ICH therapeutics.
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Acta Neurochir. Suppl. · Jan 2006
Magnesium restores altered aquaporin-4 immunoreactivity following traumatic brain injury to a pre-injury state.
Magnesium reduces edema following traumatic brain injury (TBI), although the associated mechanisms are unknown. Recent studies suggest that edema formation after TBI may be related to alterations in aquaporin-4 (AQP4) channels. In this study, we characterize the effects of magnesium administration on AQP4 immunoreactivity following TBI. ⋯ In untreated animals, AQP4 immunoreactivity was increased in the subependymal inner glia limitans and the subpial outer glia limitans, and decreased in perivascular astrocytic processes in the cerebrum and brain stem. In contrast, animals treated with magnesium sulphate had AQP4 profiles similar to normal and sham control animals. We conclude that magnesium decreases brain edema formation after TBI, possibly by restoring the polarized state of astrocytes and by down-regulation of AQP4 channels in astrocytes.