Pain
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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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Comparative Study Clinical Trial
Secondary hyperalgesia to mechanical but not heat stimuli following a capsaicin injection in hairy skin.
A psychophysical investigation was carried out to examine whether heat hyperalgesia exists within the secondary mechanical hyperalgesia zone surrounding a capsaicin injection site on hairy skin. A non-contact laser stimulator was used to deliver temperature controlled stimuli to sites within and outside the zone of mechanical hyperalgesia. Heat testing was carried out before and after the intradermal injection of 50 micrograms of capsaicin into the volar forearm. ⋯ Thus, there was no evidence for heat hyperalgesia within the zone of secondary hyperalgesia to punctate mechanical stimuli. Though the areas of punctate and stroking hyperalgesia were correlated, no correlation existed between the magnitude of capsaicin evoked pain and the areas mechanical hyperalgesia to punctuate and stroking stimuli or the area of flare. This suggests that independent mechanisms may mediate evoked pain, central sensitization that leads to mechanical hyperalgesia, and axon reflexive flare.
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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.
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Plasma and cerebrospinal fluid (CSF) steady-state concentrations (Css) of morphine (M) and the main metabolites morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G), were determined by high performance liquid chromatography (HPLC) in 21 cancer patients treated with chronic subcutaneous morphine infusion. There was a moderate, but statistically significant correlation between the daily dose of morphine and the concentrations of morphine, M3G and M6G in CSF. A poorer correlation to concentrations were seen in plasma. ⋯ Plasma and CSF concentrations of M3G and CSF concentrations of M6G correlated with administered morphine dose. There was an accumulation of both morphine glucuronides in patients with elevated serum creatinine. Measurements of morphine, M3G and M6G in CSF did not show any overt relationship to analgesia or side effects.