Articles: analgesics.
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Cancer pain remains a major cause of suffering. Improvements in its management have made unrelieved cancer pain unacceptable. While pharmacotherapy is the mainstay of cancer pain treatment, other options such as radiotherapy, nerve blocks, etc., have to be considered as well. ⋯ Anxiolytics and major tranquillisers should be avoided because they cause sedation without improving quality of analgesia. Calcitonin, diphosphonates and spasmolytics are of minor importance in this regard. Finally, concomitant medication to treat side effects of the therapy may be necessary in formulating a comprehensive treatment plan.
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Nonsteroidal anti-inflammatory drugs (NSAIDs) are very effective for the management of acute postoperative pain. These agents can be used in combination with opioid analgesics and local anaesthetics for the relief of severe postoperative pain, when the combination results in reduced narcotic requirements and improved analgesia compared with opioids and/or local anaesthetics. ⋯ By adding the NSAIDs to a routine analgesic armamentarium the goal of preventing or eliminating postoperative pain, rather than treating or reducing postoperative pain, is achieved. To use these agents more effectively, further research is required to distinguish the differences between the various NSAIDs, the optimal dosage schedules and route of administration, and, finally, the cost-effectiveness and impact on the quality and speed of postoperative recovery of NSAIDs.
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Eur. J. Clin. Pharmacol. · Jan 1992
Clinical Trial Controlled Clinical TrialPharmacokinetic-pharmacodynamic modeling of the effects of clonidine on pain threshold, blood pressure, and salivary flow.
Although clonidine analgesia appears to be mediated by the same central alpha 2-adrenoceptors that mediate its hypotensive effect, it is short-lasting when compared to the fall in blood pressure. This has been investigated by combined pharmacokinetic-pharmacodynamic analysis in 10 healthy volunteers who received (double-blind and crossover) clonidine 200 micrograms orally + placebo i.v. and clonidine orally + naloxone i.v. (2.8 mg/5 h). Analgesia was assessed by measuring the subjective (VAS) and objective (RIII) pain thresholds after transcutaneous electrical stimulations of the sural nerve; the mean arterial blood pressure (MAP), salivary flow (SF), and plasma clonidine concentrations were also monitored. ⋯ The concentration-effect curves for RIII had the same shape as MAP but the starting hysteresis suddenly collapsed, suggesting acute tolerance. The best fit was obtained with a model where the linear relationship between concentration in the effect compartment and analgesia changed acutely after the third hour. The short-lived analgesia was probably related to an acute change in pain sensitivity induced by food, suggesting that it is not mediated solely by the alpha 2-adrenoceptors responsible for hypotension.
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Clinical Trial Controlled Clinical Trial
Acute tryptophan depletion blocks morphine analgesia in the cold-pressor test in humans.
The effects of depletion of the serotonin precursor, L-tryptophan, on the threshold and tolerance to cold pressor pain, and the analgesic effect of morphine (10 mg intramuscularly), were tested in a double blind trial on human volunteers. Effects on mood were also assessed using the Profile of Mood States and the Addiction Research Center Inventory (ARCI) Scales. To deplete tryptophan, subjects were fed a tryptophan-deficient amino acid mixture 4.5 h before morphine was administered. ⋯ In subjects with normal tryptophan, the analgesic effect of morphine was predicted by the level of plasma morphine-6-glucuronide, but not by the level of morphine. Morphine increased scores on the LSD scale of the ARCI, but had no effect on other measures of mood. Tryptophan depletion also failed to alter mood in these subjects, who had unusually low depression scores before tryptophan depletion.