Der Schmerz
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Neuropeptides, such as calcitonin gene-related peptide (CGRP), substance P and vasoactive intestinal polypeptide (VIP) are considered important mediators in primary headaches. Increased concentrations of CGRP have been found in jugular venous plasma during attacks of migraine and, concomitant with VIP elevation, during cluster headache. Substance P and CGRP are produced from subsets of trigeminal afferents whereas VIP derives from parasympathetic efferents. ⋯ The activity of spinal trigeminal neurons is a sensitive integrative measure of trigeminal activity and CGRP released from central terminals of trigeminal afferents in the spinal trigeminal nucleus has been shown to facilitate nociceptive transmission, most likely by a presynaptic action. The proposed CGRP functions are supported by the distribution of CGRP receptor components localized in the rat cranial dura mater, the trigeminal ganglion and the spinal trigeminal nucleus. The currently available data indicate multiple sites of CGRP action in trigeminal nociception and the pathogenesis of migraine but central CGRP receptors are probably the essential targets in the treatment of migraine using CGRP receptor antagonists.
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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?
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The intensity of pain cannot be measured directly but can only be described subjectively. This obviously complicates the assessment especially in the younger age group. Pain evaluation and documentation are essential for good results in pain therapy. ⋯ In neonates and children up to 4 years of age, standardized scales have been developed for observation of their activities. Children in the age group 4-6 years old are able to communicate about pain. At this age self-report scales can be used to assess pain sensations."Quality Improvement in Postoperative Pain Management in Infants" (QUIPSInfant) represents a new tool for pediatric outcome evaluation, consisting of standardized data acquisition of outcome and process quality indicators.
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Postoperative pain assessment in children with cognitive impairment poses major challenges to healthcare professionals. Children with moderate to severe cognitive impairment are generally unable to communicate effectively and to self-report the level of pain. Difficulties assessing pain have led to their exclusion from clinical trials and rendered them vulnerable to insufficient treatment of pain. ⋯ Scales based on a child's own perception of pain and its severity play a limited role in this vulnerable population and pain assessment tools which rely on observing pain behavior are essential. The r-FLACC, which is reliable and valid, includes specific behavioral descriptors and can be used simply and effectively postoperatively in clinical practice. Our task has to be assessing pain as a routine procedure in cognitively impaired children as a keystone for an improved and successful pain management in this very sensitive patient population.
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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.