European journal of pain : EJP
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Previous research has clearly demonstrated a link between chronic pain and poor health, and has suggested a link with increased mortality, though the latter is less consistent. In 1996 a cohort of 6940 individuals was recruited, and information collected, about reported chronic pain status, general health and socio-demographic details. Ten years later, a record linkage was conducted between these data and the routinely collected national dataset for death registration. ⋯ After adjustment for socio-demographic factors and reported long-term limiting illness, severe chronic pain remained significantly associated with all-cause mortality (HR 1.49, 99% CI 1.21-1.84) and all circulatory system disease deaths (HR 1.68, 99% CI 1.20-2.35). The evident association between any chronic pain and increased mortality can apparently be explained by confounding caused by socio-demographic factors. However, severe chronic pain is associated with increased risk of mortality, independent of socio-demographic factors.
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Protease-activated receptor-2 (PAR-2) is a G-protein-coupled receptor activated through proteolytic cleavage. It is localized on epithelial, endothelial and inflammatory cells, as well as on transient receptor potential vanilloid 1 (TRPV1) receptor-expressing neurones. It plays an important role in inflammatory/nociceptive processes. ⋯ The inactive peptide, LRGILS-NH(2), injected into either site did not induce any inflammatory or nociceptive changes. These data provide evidence for a significant role of TRPV1 receptors in secondary mechanical hyperalgesia/allodynia and spontaneous pain induced by PAR-2 receptor activation in the knee joint. Although intraplantar PAR-2 activation-induced oedema is also TRPV1 receptor-mediated, primary mechanical hyperalgesia, impaired weight distribution and IL-1beta production are independent of this channel.
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Visceral afferents originating from different gut-segments converge at the spinal level. We hypothesized that chemically-induced hyperalgesia in the oesophagus could provoke widespread visceral hypersensitivity and also influence descending modulatory pain pathways. Fifteen healthy volunteers were studied at baseline, 30, 60 and 90 min after randomized perfusion of the distal oesophagus with either saline or 180 ml 0.1M HCl+2mg capsaicin. ⋯ Conversely, hypoalgesia to electrical stimulation, decreases in referred pain and latencies of evoked brain potentials was seen. This outcome may reflect a counterbalancing activation of descending inhibitory pathways. As these findings are also seen in the clinical setting, the model may be usable for future basic and pharmacological studies.
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The aim of the study was to explore the analgesic effect of the N-methyl-d-aspartate receptor (NMDAR) antagonist ketamine in acute experimental versus chronic spontaneous pain in Complex Regional Pain Syndrome type 1 (CRPS-1) patients. ⋯ The data indicate that while ketamine's effect on acute experimental pain is driven by pharmacokinetics, its effect on CRPS pain persisted beyond the infusion period when drug concentrations were below the analgesia threshold for acute pain. This indicates a disease modulatory role for ketamine in CRPS-1 pain, possibly via desensitization of NMDAR in the spinal cord or restoration of inhibitory sensory control in the brain.