Pain
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Clinical studies of short duration have demonstrated that strong opioids improve pain control in selected patients with chronic nonmalignant pain. However, high discontinuation rates and dose escalation during long-term treatment have been indicated. The aim of the present study was to determine discontinuation rates, dose escalation, and patterns of co-medication with benzodiazepines. ⋯ High annual doses of opioids were associated with high annual doses of benzodiazepines at the end of follow-up. It is an issue of major concern that large dose escalation is common during long-term treatment, and that that high doses of opioids are associated with high doses of benzodiazepines. These findings make it necessary to question whether the appropriate patient population receives long-term opioid treatment.
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Pain is known to play an important role in the pathway to becoming work disabled, in particular for award of disability pensions (DP) due to musculoskeletal diagnoses (MSD). This prospective cohort study investigated MSD-related pain stability and/or changes as predictors for DP during a 23-year follow-up. Additionally confounding factors were examined to elucidate whether familial effects (including genetics and family background) or socioeconomic status, other pain, or use of medication would affect the associations between pain and DP. ⋯ Musculoskeletal pain impairing work ability both measured at 1 time point and 6 years apart, and either 1 pain location or multiple locations, predicted increased risk for DP due to MSD, OA, and LBD. The associations were independent of familial confounding factors and of several influential background factors, including headache; migraine; use of analgesics, hypnotics, or tranquillizers; life satisfaction; and education and marital status. This study concluded that musculoskeletal pain impairing work ability is an early and direct predictor for DP due to MSD, OA, and LBD.
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There is evidence that inflammatory processes are involved in at least the early phase of complex regional pain syndrome (CRPS). We compared a panel of pro- and antiinflammatory cytokines in skin blister fluids and serum from patients with CRPS and patients with upper-limb pain of other origin (non-CRPS) in the early stage (< 1 year) and after 6 months of pain treatment. Blister fluid was collected from the affected and contralateral nonaffected side. ⋯ Blister fluid of CRPS patients showed a bilateral proinflammatory cytokine profile. This profile seems to be relevant only at the early stage of CRPS. Almost all measured cytokine levels were comparable to those of non-CRPS patients after 6 months of analgesic treatment and were not related to treatment outcome.
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The current study applied a model of pain communication to examine the distinction between verbal and nonverbal pain expression in their prediction of punishing, empathic, and solicitous spouse responses to patient pain. It was hypothesized that on days when patients engaged in more nonverbal expression, spouses would respond more positively (ie, with less punishing and more solicitous and empathic behavior). The same pattern was predicted for verbal expression. ⋯ The predicted positive main effect of nonverbal expression on empathic and solicitous responses was supported by the data, as was the positive main effect for verbal pain expression. Results from moderation analyses partially supported our hypothesis in that patients' nonverbal pain expression was even more strongly related to empathic and solicitous spouse responses on days of high verbal pain expression, and patients were buffered from spouse punishing responses on days when both nonverbal and verbal expression were high. These findings suggest that pain expression in both verbal and nonverbal modes of communication is important for positive and negative spousal responses.
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Calcineurin (protein phosphatase 3) regulates synaptic plasticity in the brain. The development of neuropathic pain appears dependent on some of the same mechanisms that underlie brain synaptic plasticity. In this study, we examined whether calcineurin regulates chronic constriction injury (CCI)-elicited plasticity in the spinal dorsal horn. ⋯ CCI may elicit neuropathic pain at least in part as a result of the loss of calcineurin-mediated dephosphorylation in the dorsal horn. Addition of the phosphatase by intrathecal injection reverses the injury-elicited loss and provides prolonged pain relief. Clinical therapy with calcineurin may prove to be a novel, effective, and safe approach in the management of well-established neuropathic pain.