Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Oct 2008
Patient-controlled epidural analgesia (PCEA) for postoperative pain control after lumbar spine surgery.
Spine surgery remains one of the most common procedures for patients with a wide variety of spine disorders. Postoperative pain after major spine surgery is moderate to severe. We retrospectively reviewed 245 medical records of adult patients undergoing major spine surgery who received either patient-controlled epidural analgesia based on local anesthetics and opioids or patient-controlled intravenous analgesia as postoperative pain management. ⋯ The use of a reduced amount of opioids by patients with epidural analgesia may be relevant because of potential fewer side effects mainly in elderly patients. Several limitations related to the retrospective nature of the study are described. Prospective randomized-controlled trials are needed to understand and elucidate the optimum regimen of postoperative pain management after major spine surgery.
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J Neurosurg Anesthesiol · Oct 2008
Evaluation of a bedside monitor of regional CBF as a measure of CO2 reactivity in neurosurgical intensive care patients.
Mild hyperventilation remains a key element in the management of elevated intracranial pressure. However, a harmful effect of hyperventilation on the development or deterioration of ischemic lesions has been shown in patients after severe head trauma. The objective of this study was to investigate the clinical feasibility and reliability of continuous monitoring of regional cerebral blood flow (rCBF) during mild hyperventilation using a thermodiffusion probe. CO2 reactivity was calculated. The measurement of the partial pressure of oxygen (PtiO2) in the cerebral tissue served as a reference parameter. ⋯ Continuous monitoring of regional CBF, using an intraparenchymally placed thermodiffusion probe, seems to be a simple and safe bedside technique. The promise of reliably monitoring and interpreting additional parameters such as PtiO2 and PtiCO2 warrants further investigation.
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J Neurosurg Anesthesiol · Oct 2008
N-methyl-D-aspartate (NMDA) antagonists--S(+)-ketamine, dextrorphan, and dextromethorphan--act as calcium antagonists on bovine cerebral arteries.
Ketamine, an intravenous anesthetic and a major drug of abuse, is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist. Ketamine's enantiomer, S(+)-ketamine, acts stereoselectively on neuronal NMDA receptors. The purpose of this in vitro study was to compare the direct effects of S(+)-ketamine, 2 other noncompetitive NMDA receptor antagonists (dextrorphan and dextromethorphan), and the calcium entry blocker nimodipine on the cerebral vasculature, using bovine middle cerebral arteries as an experimental model. ⋯ In additional experiments, arterial strips were mounted in isolated tissue chambers to directly measure calcium uptake, using 45calcium (45Ca) as a radioactive tracer. The NMDA antagonists and nimodipine each blocked potassium-stimulated or U46619-stimulated Ca2+ uptake into arterial strips. These results indicate that S(+)-ketamine, dextrorphan, and dextromethorphan, like nimodipine, directly dilate cerebral arteries by acting as calcium antagonists; they all inhibit 45Ca uptake through both potential-operated (potassium) and receptor-operated (U46619) channels in cerebrovascular smooth muscle.
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Certain anesthetics exhibit neurotoxicity in the brains of immature but not mature animals. Gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the adult brain, is excitatory on immature neurons via its action at the GABAA receptor, due to a reversed transmembrane chloride gradient. GABAA receptor activation in immature neurons is sufficient to open L-type voltage-gated calcium channels. ⋯ Both muscimol and propofol induced a rapid increase in [Ca2+]i in days in vitro (DIV) 4, but not in DIV 8 neurons, that was inhibited by nifedipine and bicuculline. Caspase-3,-7 activities and cell death increased significantly in DIV 4 but not DIV 8 hippocampal neuronal cultures 1 hour after 5 hours exposure to propofol, but not muscimol, and were inhibited by the presence of bicuculline or nifedipine. We conclude that an increase in [Ca2+]i, due to activation of GABAA receptors and opening of L-type calcium channels, is necessary for propofol-induced death of immature rat hippocampal neurons but that additional mechanisms not elicited by GABAA activation alone also contribute to cell death.