The journal of pain : official journal of the American Pain Society
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Multicenter Study Clinical Trial
Initial Psychometric Properties of the Pain Care Quality Survey (PainCQ).
This study examined the psychometric properties of the Pain Care Quality (PainCQ) survey, a new instrument to measure the quality of nursing and interdisciplinary care related to pain management. Hospitalized medical/surgical oncology patients with pain from 3 states completed the 44-item version of the PainCQ survey following completion of a nursing shift. Interdisciplinary items were evaluated over the entire hospital stay; nursing care was evaluated during the previous shift. The sample included 109 patients ranging in age from 20 to 84 (mean = 53.09). The sample was 58.7% female, 88% non-Hispanic white. Principal Axis Factoring with an oblimin rotation was used as factors were correlated. Two scales resulted. The PainCQ-Interdisciplinary scale included 11 items representing 2 constructs and explaining 47.1% of shared item variance: partnership with the health care team (k = 6 items; α = .85) and comprehensive interdisciplinary pain care (k = 5 items; α = .76). The PainCQ-Nursing scale measured three constructs and explained 60.8 % of shared item variance: being treated right (k = 15 items; α = .95), comprehensive nursing pain care (k = 3 items; α = .77), and efficacy of pain management (k =4 items; α = .87). Results supported the internal consistency reliability and structural validity of the PainCQ survey with 33 items. ⋯ This article presents the psychometric properties of a new tool to measure interdisciplinary and nursing care quality related to pain management from the patient's perspective. This tool can be used for research and as a clinical performance measure to monitor and improve quality of care and patient outcomes.
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Randomized Controlled Trial
Therapeutic Interactive Voice Response (TIVR) to reduce analgesic medication use for chronic pain management.
This paper examines whether a telephone-based, automated maintenance enhancement program can help to reduce opioid and nonsteroidal anti-inflamatory drugs (NSAID) analgesic use in patients with chronic pain. Following 11 weeks of group cognitive-behavioral therapy (CBT), 51 subjects with chronic musculoskeletal pain were randomized to 1 of 2 study groups. Twenty-six subjects participated in 4 months of a Therapeutic Interactive Voice Response (TIVR) program in addition to standard follow-up care, while a control group of 25 subjects received standard follow-up care only. TIVR is an automated, telephone-based tool developed for the maintenance and enhancement of CBT skills. Opioid analgesic use decreased in the experimental group in both follow-ups: 4 and 8 months postCBT. In addition, at 8-month follow-up, 21% of the TIVR subjects had discontinued the use of opioid analgesics, 23% had discontinued NSAIDS, and 10% had discontinued antidepressant medications. In contrast, the control group showed increases in opioid and NSAIDS use. Analysis of covariance (ANCOVA) revealed significant between-group differences in opioid analgesic use at 8-month follow up (P = .004). We have previously demonstrated the efficacy of TIVR to decrease pain and improve coping; this analysis demonstrates that the use of TIVR may also result in concurrent reductions in opioid analgesic and NSAID medications use. ⋯ This article demonstrates that the Therapeutic Interactive Voice Response maintenance enhancement program can help to reduce opioid analgesic use in patients with chronic pain. This automated maintenance enhancement program could potentially assist patients not only to decrease pain and improve coping, but also to diminish the likelihood of opioid dependence.
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The endocannabinoids anandamide and 2-arachidonoylglycerol are predominantly regulated by the respective catabolic enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). Inhibition of these enzymes elevates endocannabinoid levels and attenuates neuropathic pain. In the present study, CB₁ and CB₂ receptor-deficient mice were subjected to chronic constriction injury (CCI) of the sciatic nerve to examine the relative contribution of each receptor for the anti-allodynic effects of the FAAH inhibitor, PF-3845, and the MAGL inhibitor, JZL184. CCI caused marked hypersensitivity to mechanical and cold stimuli, which was not altered by deletion of either the CB₁ or CB₂ receptor, but was attenuated by gabapentin, as well as by each enzyme inhibitor. Whereas PF-3845 lacked anti-allodynic efficacy in both knockout lines, JZL184 did not produce anti-allodynic effects in CB₁ (-/-) mice, but retained its anti-allodynic effects in CB₂ (-/-) mice. These data indicate that FAAH and MAGL inhibitors reduce nerve injury-related hyperalgesic states through distinct cannabinoid receptor mechanisms of action. In conclusion, although endogenous cannabinoids do not appear to play a tonic role in long-term expression of neuropathic pain states, both FAAH and MAGL represent potential therapeutic targets for the development of pharmacological agents to treat chronic pain resulting from nerve injury. ⋯ This article presents data addressing the cannabinoid receptor mechanisms underlying the anti-allodynic actions of endocannabinoid catabolic enzyme inhibitors in the mouse sciatic nerve ligation model. Fatty acid amide hydrolase and monoacylglycerol lipase inhibitors reduced allodynia through distinct cannabinoid receptor mechanisms. These enzymes offer potential targets to treat neuropathic pain.
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The protein kinase mammalian target of rapamycin (mTOR) regulates mRNA translation and is inhibited by rapamycin. Signaling pathways involving mTOR are implicated in physiological and pathophysiological processes. We determined the spinal effects of the rapamycin analogue cell cycle inhibitor (CCI)-779 on neuronal responses and behavioral hypersensitivity in a model of persistent neuropathic pain. We also assessed the anatomical distribution of spinal mTOR signaling pathways. Specifically, we ligated rat spinal nerves L5 and L6 to produce a model of neuropathic pain. After confirming neuropathy with behavioral testing, we obtained in vivo single-unit extracellular stimulus-evoked recordings from deep dorsal horn spinal neurons. We applied CCI-779 spinally in electrophysiological and behavioral studies and assessed its effects accordingly. We also used immunohistochemistry to probe for mTOR signaling pathways in dorsal root ganglia (DRG) and the spinal cord. We found that spinally administered CCI-779 rapidly attenuated calibrated mechanically but not thermally evoked neuronal responses and mechanically evoked behavioral responses. Immunohistochemistry showed presence of mTOR signaling pathways in nociceptive-specific C-fiber DRG and in neurons of inner lamina II of the spinal cord. We conclude that alterations in the activity of spinal mTOR signaling pathways are crucial to the full establishment of spinal neuronal plasticity and behavioral hypersensitivity associated with nerve injury. ⋯ This study is consistent with growing evidence implicating mTOR signaling pathways as important modulators of persistent pain, providing novel insights into the molecular mechanisms of pain maintenance and potential for novel approaches into treating chronic pain.
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The central nucleus of the amygdala (CeA) is involved in processing and regulation of pain. We determined whether amygdaloid corticotropin-releasing factor (CRF) contributes to pain modulation in the neuropathic rat. Emotional aspect of pain was assessed by an aversive place-conditioning test and sensory aspect of pain by determining monofilament-induced limb-withdrawal threshold. CRF₆₋₃₃ (an inhibitor of CRF-binding protein) or CRF₉₋₄₁, a nonselective CRF receptor antagonist, was microinjected to the left or right CeA or a control site in rats with spared nerve injury (SNI) or sham operation of the left hind limb. In SNI animals, CRF₆₋₃₃ in the left or right CeA, but not in a control site, attenuated emotional painlike behavior and increased sensory pain. In sham controls, CRF₆₋₃₃ in the right but not left CeA increased sensory aspect of pain, without influence on place-avoidance behavior. The effects induced by CRF₆₋₃₃ were reversed by CRF₉₋₄₁. The results indicate that endogenous CRF in the CeA, through action on CRF receptors, may differentially influence emotional and sensory aspects of pain in neuropathy. While the right CeA had a dominant role in modulation of pain-related responses in sham controls, left as well as right CeA contributed to pain modulation in neuropathic animals. ⋯ An increase in free endogenous corticotropin-releasing factor in the central nucleus of the amygdala was accompanied by increased cutaneous hypersensitivity and decreased emotional painlike behavior in neuropathic animals. This finding indicates that CRF in the amygdala may have differential effects on sensory and emotional aspects of neuropathic pain.