Pain
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Chronic pain has adverse effects on individuals with chronic pain (ICPs) as well as their family members. Borrowing from an empathy model described by Goubert et al. (2005), we examined top-down and bottom-up factors that may be related to psychological well-being in the spouses of ICPs. A diverse community sample of 113 middle-aged spouses of individuals with chronic pain (ICPs) completed measures on pain severity and spouse pain catastrophizing (PCS-S; Cano et al., 2005). ⋯ However, when both partners reported chronic pain, there was no significant difference in psychological distress between partners. Hierarchical regression analyses showed that spouse magnification catastrophizing was associated with depressive and anxiety symptoms, and that helplessness catastrophizing was associated with depressive symptoms for spouses of ICPs who also reported chronic pain but not for spouses of ICPs without chronic pain. The results are discussed in light of interpersonal processes that may affect spouses' distress.
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Lidocaine-like sodium channel blocking drugs provide pain relief either by interrupting impulse conduction in neurons when applied locally in high concentrations or, when given systemically, by suppressing high-frequency ectopic discharges due to preferential drug binding to inactivated channel states. Lidocaine-like actions of opioids have frequently been demonstrated clinically. However, drug binding to resting and inactivated channel conformations has been studied systematically only in the case of meperidine. ⋯ Sufentanil, fentanyl and tramadol but not morphine reversibly suppressed sodium inward currents at high concentrations (half-maximum blocking concentrations (IC50) 49+/-4, 141+/-6 and 103+/-8 microM) when depolarizations were started from hyperpolarized holding potentials. Short depolarizations inducing fast-inactivation and long prepulses inducing slow-inactivation significantly (*p < or = 0.001) increased the blocking potency for these opioids. 15% slow inactivated channels reduced the respective IC50 values to 5+/-3, 12+/-2 and 21+/-2 microM. These results show that: (1) Sufentanil, fentanyl and tramadol block voltage-gated sodium channels with half-maximum inhibitory concentrations similar to the IC50 reported for meperidine. (2) Slow inactivation--a physiological mechanism to suppress ectopic activity in response to slow shifts in membrane potential--increases binding affinity for sufentanil, fentanyl and tramadol. (3) Morphine has no such effects.
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Inflammation, peripheral nerve injury and chemical irritants can cause central sensitization in pain pathways. Prostaglandins produced in the CNS induce central sensitization during inflammation mainly by relieving nociceptive neurons from glycinergic inhibition. We have recently identified spinal prostaglandin E receptors of the EP2 subtype (EP2 receptors) and the glycine receptor alpha3 subunit (GlyR alpha3) as signal transduction elements involved in the generation of central inflammatory hyperalgesia. ⋯ The lack of a phenotype in GlyR alpha3-/- mice together with the absence of a facilitating effect of intrathecal PGE2 on formalin-induced nociception in wild-type mice suggests that peripheral rather than spinal EP2 receptors are involved. These results indicate that inhibition of glycinergic neurotransmission by EP2 receptor activation does not contribute to pain following peripheral nerve injury or chemical irritation with formalin. Our results thus provide further evidence that inflammatory hyperalgesia and neuropathic pain involve different mechanisms of central sensitization.
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Studies implicate endocannabinoids in the acute and chronic actions of opioid drugs, including the genesis of physical dependence. Previous evidence suggests that spinal release of calcitonin gene-related peptide (CGRP) and activation of its receptors contribute to opioid physical dependence. The release of CGRP at the spinal level is modulated by cannabinoid (CB1)-receptors. ⋯ Intrathecal co-administration of CB1-receptor antagonists, AM-251 or SR141716A, with daily morphine attenuated the behavioral manifestations of withdrawal. Treatment with AM-251 also reduced the depletion of CGRP, suppressed Fos-induction, and prevented the increase in capsaicin-evoked spinal CGRP release. Altogether, this study suggests that endocannabinoid activity, expressed via CB1-receptors, contributes to the induction of opioid physical dependence through spinal modulation of CGRP.
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Clinical Trial
The influence of communication goals and physical demands on different dimensions of pain behavior.
The purpose of the present research was to examine the influence of communication goals and physical demands on the expression of communicative (e.g., facial grimaces) and protective (e.g., guarding) pain behaviors. Participants with musculoskeletal conditions (N=50) were asked to lift a series of weights under two communication goal conditions. In one condition, participants were asked to estimate the weight of the object they lifted. ⋯ The results of this study support the functional distinctiveness of different forms of pain behavior. Findings are discussed in terms of evolutionary and learning theory models of pain behavior. Clinical implications of the findings are addressed.