Pain
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A midline dorsal column lesion has been shown to be an effective surgical treatment for the relief of pelvic visceral pain in patients. The aim of this study was to examine the effectiveness of a dorsal column lesion upon: (i) increased electrophysiological responses of neurons in the ventral posterolateral thalamic nucleus in anesthetized rats evoked by the application of bradykinin to the surface of the pancreas, and (ii) pain-related behaviors observed after pancreatic infusion with bradykinin. In rats anesthetized with pentobarbital, recordings from individual thalamic neurons were made using tungsten electrodes. ⋯ A dorsal column lesion made prior (1 week) to the bradykinin infusion reduced the decrease in exploratory behavior but did not return exploratory behavior to control levels. In conclusion, nociceptive information relayed to the thalamus about the pancreas is transmitted from the spinal cord through the dorsal columns, possibly by the post-synaptic dorsal column pathway. However, the dorsal column pathway may not be the sole route for relaying information about noxious stimulation of the pancreas, particularly that impacting complex behavioral responses.
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Recent studies suggest that opioids can produce analgesia through peripheral mechanisms following inflammation of peripheral tissue. This study examined whether opioids administered prior to inflammation can produce antinociception by peripheral mechanisms in a model of visceral pain. Mice were injected intraperitoneally (i.p.) with 1% acetic acid to evoke abdominal writhing, a standard model of visceral pain. ⋯ The highest dose (10 microg) was ineffective when given intravenously 5 min before acetic acid, suggesting that antinociception following i.p. administration was acting via peripheral mechanisms. These data demonstrate that low doses of opioids, given before or after acetic acid, produce visceral antinociception through peripheral mechanisms. This may be clinically relevant for the management of postoperative abdominal pain.
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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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One of the most commonly used experimental animal models for neuropathic pain is the chronic constriction injury (CCI) where four loose ligatures are tied around the sciatic nerve. One disadvantage of this model is the introduction of foreign material into the wound, which causes a local inflammatory reaction. Thus the distinction between the neuropathic and the inflammatory component of pain is difficult in this model. ⋯ In the epineurium the number of macrophages was strikingly increased after CCI compared with PST, indicating that the response of the immune system is different in a structural lesion with and without foreign material. In conclusion, PST is a pure nerve injury model without an epineurial inflammatory component due to foreign material and is therefore well suited for studying the role of local endoneurial processes in the development and maintenance of neuropathic pain. Also, the importance of regeneration in the termination of hyperalgesia can convincingly be shown in this model.