Der Schmerz
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Review Comparative Study
[Serotonin receptor 1A-modulated dephosphorylation of glycine receptor α3: a new molecular mechanism of breathing control for compensation of opioid-induced respiratory depression without loss of analgesia].
To control the breathing rhythm the medullary respiratory network generates periodic salvo activities for inspiration, post-inspiration and expiration. These are under permanent modulatory control by serotonergic neurons of the raphe which governs the degree of phosphorylation of the inhibitory glycine receptor α3. ⋯ Our physiological investigations show that this 5-HTR(1A)-GlyRα3 modulation allows treatment of respiratory depression due to opioids without affecting the desired analgesic effects of opioids. The molecular mechanism presented here opens new pharmacological possibilities to treat opioid-induced respiratory depression and respiratory disorders due to disturbed inhibitory synaptic transmission, such as hyperekplexia.
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Meta Analysis Comparative Study
Meta-analysis of dropout rates in randomized controlled clinical trials: opioid analgesia for osteoarthritis pain.
The interpretation of opioid studies in patients with chronic pain due to osteoarthritis is limited by a high dropout rate. Therefore, the implication of dropouts on the recommendation of opioids in chronic osteoarthritis pain was analyzed. ⋯ In spite of analgesic effects, many osteoarthritis patients prefer to stop chronic opioid use, because of adverse events. Therefore, opioids are not generally recommended in osteoarthritis.
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Randomized Controlled Trial Comparative Study
[Clonidine for remifentanil-induced hyperalgesia: a double-blind randomized, placebo-controlled study of clonidine under intra-operative use of remifentanil in elective surgery of the shoulder].
In the postoperative period, α2-adrenergic agonists have an opioid sparing effect. In a previous, experimental study, it was also shown that clonidine attenuates remifentanil-induced hyperalgesia. In this study, we examined under clinical conditions whether early administration of a single dose of clonidine can inhibit remifentanil-induced hyperalgesia in patients undergoing elective surgery of the shoulder and with continuous intraoperative use of remifentanil. ⋯ An early single dose of 150 µg of clonidine did not reduce the postoperative morphine consumption and pain scores in patients undergoing elective surgery of the shoulder with remifentanil/propofol-based anaesthesia. After the effect of clonidine has presumably subsided the pain can even increase, therefore further studies with repetitive doses of clonidine should be carried out.
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This contribution compares unexplained essential questions regarding the placebo response with current empirical evidence: (1) Are the placebo response rates equivalent in the groups treated with medication or placebo? Very little evidence has been gathered to support this generally accepted additivity while some findings negate its validity. (2) Is the placebo response a function of the probability of receiving medication or placebo? There are indications that the number of study groups included in a trial determines the level of placebo and medication response. (3) How great is the placebo response in trials that directly compare a (new) medication with one that for example is already on the market? There are indications that such comparative studies produce higher placebo response rates. (4) How high is the placebo response rate in everyday clinical practice--or does the response to a medication in trials substantiate the effect of the medication in everyday clinical practice?