Pain
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Evidence from animal models and studies of human sensory nerves demonstrate that tetrodotoxin (TTX)-resistant Na(+) channels are present in sensory neurons and might play an important role in pain conduction and chronic pain. Recent investigations suggest that TTX-resistant Na(+) channels in the peripheral nervous system are less sensitive to local anesthetics than TTX-sensitive Na(+) channels. To test the effects of the clinically used local anesthetics lidocaine and bupivacaine on TTX-resistant action potentials (APs) in sensory neurons, we performed electrophysiological experiments on small dorsal root ganglion (DRG) neurons from young rats. ⋯ Time to peak and duration of TTX-resistant APs were prolonged by local anesthetics. Trains of APs could be elicited in some neurons by long-lasting current injections, and the half-maximal concentrations needed to suppress these trains were 30 microM lidocaine or 10 microM bupivacaine. We suggest that the reduction in firing frequency at low concentrations of local anesthetic may explain the phenomenon of paresthesia when sensory information is gradually suppressed during spinal anesthesia.
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Randomized Controlled Trial Clinical Trial
Expectations of analgesia do not affect spinal nociceptive R-III reflex activity: an experimental study into the mechanism of placebo-induced analgesia.
The purpose of this study was to investigate whether placebo analgesia is mediated by the release of beta-endorphin. In addition to subjective pain reports, we included an objective physiological parameter of nociception reflected by the opioid sensitive nociceptive R-III reflex. Placebo consisted of strong suggestions of pain relief and an intravenous injection of saline. ⋯ Consistently, the antagonizing effects of naloxone were negligible. A subgroup analysis of those who did show a placebo response as indicated on the VAS did not support the supposition that beta-endorphin is released due to placebo suggestion. It is suggested that intensified stimuli and a more effective procedure to induce placebo analgesia (e.g. conditioning) may produce a proper placebo effect.
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Both physicians and nurses are responsible for adequate pain management. The aim of this study was to assess pain management behavior of physicians and nurses, and to evaluate the effects of a Pain Monitoring Program for nurses on the extent to which nurses administer analgesics. The Pain Monitoring Program consisted of two components: educating nurses about pain, pain assessment and pain management; and implementing daily pain assessment by means of a numeric rating scale. ⋯ Based on this study it can be concluded that the use of a simple method such as a numeric rating scale together with pain education for nurses is effective in improving the administration of analgesics by nurses. These are important results because nurses play an essential role in helping patients to cope with their pain. Because the Pain Monitoring Program (PMP) was effective in a heterogeneous population in multiple care settings, the possibility of implementing the PMP in routine nursing practice should be considered.
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Recent animal studies using stress-induced analgesia have suggested a general age-related decline in endogenous pain inhibitory systems. The aim of the current study was to examine age-related differences in the magnitude of endogenous analgesia in human volunteers, using psychophysical measures of neuroselective electrical, and thermal CO(2) laser induced pain thresholds, before, immediately after and 1 h after repeated cold water immersion of the hand. Sensory detection thresholds did not differ between age groups indicating that the functional integrity of primary afferent sensory fibres appears to be intact in older people. ⋯ This effect was relatively transient with thresholds returning to baseline within 1 h. The magnitude of analgesic response, however, was found to be significantly less in older people. Age differences in the efficacy of endogenous analgesic systems may be expected to reduce the ability of older adults to cope with severe persistent pain states and may help explain some of the variation in the literature on pain report.
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Comparative Study
Comparison of autotomy behavior induced in rats by various clinically-used neurectomy methods.
When a peripheral nerve is cut, a neuroma develops at its proximal end. Nerve-end neuromas are known to be a source of ectopic sensory input. In some humans this input may cause spontaneous and evoked neuropathic pain. ⋯ The differing scores of autotomy caused by these neurectomy methods may derive from different properties of the injury discharge produced by these methods at the time of nerve cut. Our results raise the possibility that a higher incidence of neuropathic pain or related sensory disorders in humans may be expected following cryosurgical and electrocut neurectomies. If validated by further studies, neurectomy methods eliciting lower incidence of autotomy, and sensory disorders in models not based on autotomy may produce lower levels of neuropathic pain in humans.