Der Schmerz
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Pain measurement during diagnostic procedures is an accepted prerequisite for appropriate therapy. In this study, the agreement between rankings of pain intensity on a numerical and a verbal rating scale was analyzed. ⋯ Both scales can be employed efficiently for pain assessment during diagnostic procedures. Verbal categories can be assigned to numerical values and vice versa numerical values to verbal categories. However, in view of the inter-individual variations it appears appropriate to re-assure pain perception with each patient in order to avoid over- or undertreatment.
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Spinal cord stimulation (SCS) is an effective alternative treatment in patients with chronic neuropathic pain and mainly radicular distribution. The aim of this prospective study was to investigate changes in BOLD signal with fMRI during active SCS and to correlate the results with the clinical pain intensity, measured with a visual analogue scale (VAS). ⋯ In patients with chronic neuropathic pain and high VAS levels, SCS elicited BOLD activation in the cingulate gyrus, thalamus, prefrontal cortex, and primary and secondary somatosensory area. Pain reduction by SCS resulted in a reduction of functional activity in these areas as revealed by follow-up fMRI.
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Recent advances in knowledge about gene structure derived from the human genome project has also revealed data on genomic variation and their possible impact on complex and acute diseases as well as pharmacotherapy. The hypothesis of a genetic predisposition for complex diseases such as pain syndromes, side effects, and adverse outcomes challenging the clinician is ready to be tested by advanced genetic-epidemiologic study designs employing the latest genotyping technology. ⋯ Genetic differences in drug kinetics and dynamics, e.g., differences in metabolism or genetic variations of the drug target (e.g., receptors) will be of importance in the future. Pharmacogenetics can individualize pharmacotherapy and improve care by predicting the optimal dose and avoiding side effects and toxicity in individual patients.
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Opioids are frequently used for the treatment of moderate to severe acute and chronic pain. However, clinical evidence suggests that opioids can elicit increased sensitivity to noxious stimuli suggesting that administration of opioids can activate both, pain inhibitory and pain facilitatory systems. Acute receptor desensitization via uncoupling of the receptor from G proteins, upregulation of the cAMP pathway, activation of the N-methyl-D-aspartate (NMDA) receptor system and descending facilitation have been proposed as potential mechanisms underlying opioid-induced hyperalgesia. ⋯ Brief exposures to mu-receptor agonists induce long-lasting hyperalgesic effects for days. Furthermore, the prolonged use of opioids in patients often requires increasing doses and may be accompanied by the development of abnormal pain. Successful strategies that may decrease or prevent opioid-induced hyperalgesia include the concomitant administration of drugs such as NMDA antagonists, alpha(2)-agonists, or nonsteroidal anti-inflammatory drugs (NSAID), opioid rotation, or combinations of opioids with different receptor selectivity.
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Opioids are valuable analgesics, capable of providing pain relief and functional improvement not only in patients with cancer-related pain, but also in chronic noncancer-related pain patients. However, recent data have shown that the increasing prescription of opioids is associated with a rise in aberrant drug-related behaviour. The causes of this behaviour are multifactorial. ⋯ Assessment of the progress of therapy is based on the following factors: analgesic efficacy, adverse side effects, functional status and aberrant drug-related behaviour. In the absence of a successful opioid therapy, the treatment must be discontinued to avoid iatrogenic damage, substance abuse and illegal diversion. After discontinuation of the therapy, a comprehensive interdisciplinary re-evaluation is required.