Pain
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N-Methyl-D-aspartate (NMDA) receptor antagonists have been shown to block the development of antinociceptive tolerance to morphine. Assessment of the effects of NMDA antagonists on development of antinociceptive tolerance to selective opioid mu (mu) and delta (delta) agonists, however, has not been reported. In these experiments, selective mu and delta receptor agonists, and morphine, were repeatedly administered to mice either supraspinally (i.c.v.) or systemically (s.c.), alone or after pretreatment with systemic NMDA antagonists. ⋯ Further, MK801 pretreatment also did not affect the development of tolerance to the antinociception resulting from a cold-water swim-stress episode, previously shown to be a delta-opioid mediated effect. These data lead to the suggestion that the mechanisms of tolerance to receptor selective mu and delta opioids may be regulated differently from those associated with morphine. Additionally, these findings emphasize that conclusions reached with studies employing morphine cannot always be extended to 'opiates' in general.
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Randomized Controlled Trial Clinical Trial
Nimodipine fails to enhance the analgesic effect of slow release morphine in the early phases of cancer pain treatment.
We assessed nimodipine's ability to increase the analgesic effect of morphine in 32 patients suffering from cancer pain in a double-blind, placebo controlled cross-over study. Morphine administration began a few days before the start of the study. The analgesic effects of two combinations were compared: morphine (M) plus placebo (P) and morphine plus 90 mg/24 h of nimodipine (N). ⋯ However, when the same statistical tests were used for comparison of results with pre-treatment baseline values, highly significant differences between mean scores on the scales for pain relief and pain intensity were found. Based on these negative results we conclude that nimodipine given orally at a dose of 30 mg every 8 h does not enhance analgesia when associated with morphine in the early phases of treatment for cancer pain. Our study also gives clear evidence of a placebo effect.
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The problem of pain following spinal cord injury challenges the health care community to develop new treatment strategies for patients requiring pain management. A number of pain syndromes are associated with spinal injury based on the nature of the lesion, neurological structures damaged, and secondary pathophysiological changes. Efforts to identify specific characteristics of each syndrome are an important beginning to the successful diagnosis and treatment of spinal injury pain. ⋯ Future research related to these hypotheses will need to focus on the use of appropriate injury models that simulate the pathological changes associated with human injuries and which lead to clinically relevant pain-related behaviors. Continued research directed towards an examination of these proposed mechanisms will also require new research strategies and a cooperative working relationship between basic and clinical scientists. In this review the clinical characteristics of spinal injury pain and the results of experimental studies are discussed.
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Clinical Trial Controlled Clinical Trial
Development and preliminary validation of a postoperative pain measure for parents.
Parents are now primarily responsible for the at home assessment and treatment of their children's pain following minor surgery. Although some research has suggested that parents underestimate their children's pain following surgery, no behavioral measure exists to assist parents in pain assessment. The Postoperative Pain Measure for Parents was developed based on cues parents reported using to assess their children's pain (e.g. changes in appetite, activity level). ⋯ This study provides preliminary evidence for the use of the Postoperative Pain Measure for Parents as a valid assessment tool with children between the ages of 7-12 years following day surgery. It is internally consistent and strongly related to child-rated pain. Future research should explore the use of this measure with a younger sample and children with developmental delays.
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Compounds related to capsaicin and its ultrapotent analog, resiniferatoxin (RTX), collectively referred to as vanilloids, interact at a specific membrane recognition site (vanilloid receptor), expressed almost exclusively by primary sensory neurons involved in nociception and neurogenic inflammation. Desensitization to vanilloids is a promising therapeutic approach to mitigate neuropathic pain and pathological conditions (e.g. vasomotor rhinitis) in which neuropeptides released from primary sensory neurons play a major role. Capsaicin-containing preparations are already commercially available for these purposes. ⋯ We further focus on ligand-induced messenger plasticity, a recently discovered mechanism underlying the analgesic actions of vanilloids. Lastly, we give a brief overview of the current clinical uses of vanilloids and their future therapeutic potential. The possibility is raised that vanilloid receptor subtype-specific drugs may be synthesized, devoid of the undesirable side-effects of capsaicin.