Pain
-
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.
-
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.
-
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.
-
Although evidence reveals that self-efficacy is associated with disability in people with pain, there is less known about this relationship in primary care settings and no published information in general population samples. This study aimed to assess the relationship between pain, self-efficacy, health-related quality of life, psychological distress and disability in a general population sample. A randomly selected sample from electoral registers of the lower North Island of New Zealand was mailed a survey questionnaire. ⋯ This interaction was not observed for health self-efficacy. General self-efficacy was more strongly related to psychological distress and this association was not influenced by pain status. Health-related quality of life was associated with health self-efficacy but not general self-efficacy.
-
While animal studies suggest that neonatal pain experiences induce long-term alterations in pain sensitivity, no such data exist in humans. Changes in pain sensitivity in school-aged children (9-14 years) who were born preterm or fullterm, had been hospitalized for a prolonged period of time after birth and had undergone repeated painful procedures while being treated in a Neonatal Intensive Care Unit (NICU) were determined. A retrospective cohort study of 19 preterm (