Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2003
Case ReportsAn unusual complication of total intravenous anesthesia: mutism.
We report a case of mutism secondary to total IV anesthesia with propofol, as an unusual complication that we have not found in the literature.
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Anesthesia and analgesia · Jan 2003
Case ReportsConversion disorder after implant of a spinal cord stimulator in a patient with a complex regional pain syndrome.
This case history describes the treatment of a patient suffering with persistent pain. He was treated surgically with implantation of a spinal cord stimulator. After surgery, a partial paralysis that could not be explained medically and that was probably related to emotional factors occurred, and cognitive behavioral treatment was begun. This paper discusses the importance of considering social and psychological factors when medical treatment options are considered.
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Anesthesia and analgesia · Jan 2003
Volatile anesthetics reduce agonist affinity at nicotinic acetylcholine receptors in the brain.
In previous studies we and others have demonstrated that the activation of nicotinic acetylcholine receptors (nAChRs) is inhibited by subanesthetic concentrations of volatile anesthetics. The mechanism by which activation is inhibited is unknown. Studies of the evolutionarily related nAChRs from the electric fish Torpedo have suggested that volatile anesthetics alter the affinity of the agonist for the receptor. We studied the effect of two volatile anesthetics, isoflurane and sevoflurane, on equilibrium binding of the high-affinity nicotinic agonist epibatidine to nicotinic receptors from mouse brain. We studied binding to male and female brain separately, because sex differences in nicotine responses have been reported. Male and female brains have equal epibatidine binding without anesthetic. Isoflurane and sevoflurane reduce the binding of [(3)H]epibatidine to male and female nicotinic receptors, but only at concentrations at and above those required for anesthesia. The 50% inhibitory concentration for isoflurane inhibition of [(3)H]epibatidine binding to male brain was 0.58 +/- 0.07 mM and to female brain was 1.62 +/- 0.30 mM. The 50% inhibitory concentration for sevoflurane inhibition of [(3)H]epibatidine binding to male brain was 0.77 +/- 0.05 mM and to female brain was 0.77 +/- 0.04 mM. There was no statistically significant difference in the effect of either drug between sexes (P > 0.05). Although there is a slight decrease in agonist affinity at anesthetic concentrations, the marked reductions in nAChR function at subanesthetic concentrations cannot be attributed to changes in agonist affinity. ⋯ Volatile anesthetics reduce the activation of nicotinic acetylcholine receptors by an unknown mechanism. We have demonstrated that although isoflurane and sevoflurane inhibit agonist affinity, the concentrations required are too large to be responsible for the dynamic changes observed.
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Although both alpha2-adrenergic agonists and cyclooxygenase inhibitors produce analgesia, their exact sites of action and interaction remain unclear. A previous report demonstrated a surprising inhibition of antinociception in rats from intrathecal clonidine by co-administered ketorolac. There are no other reports of interaction between these two classes of analgesics. We therefore reexamined this interaction, determining the effect of intrathecal clonidine and ketorolac alone and in combination in normal rats. Clonidine, but not ketorolac, produced antinociception to noxious hind paw thermal stimulation. The addition of ketorolac significantly enhanced the effect of clonidine, indicating a synergistic interaction for analgesia. Although the reasons for the discrepancy between this and the previous report are unclear, these results are consistent with previous studies that indicate an antinociceptive action of intrathecal alpha2-adrenergic agonists in the normal condition, a lack of such effect for cyclooxygenase inhibitors, and positive reinforcing effects of these two systems when co-stimulated. ⋯ Spinal injection of the alpha2-adrenergic agonist clonidine and the cyclooxygenase inhibitor ketorolac results in a synergistic interaction for antinociception in normal animals, suggesting that the combination of these drugs will enhance rather than detract from the analgesia of either alone.