European journal of pain : EJP
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There is a range of anxiety-related constructs associated with pain and pain-related disability. Those most often examined are pain catastrophizing, pain anxiety and anxiety sensitivity. All three are conceptualized to be important in the development and maintenance of chronic pain, and are included within fear avoidance models. ⋯ They completed a battery of measures related to anxiety, pain and disability. Once controlling for injury-related variables, catastrophizing was found to predict current pain, pain-related anxiety predicted task-related pain, whereas anxiety sensitivity was (negatively) associated with disability. These findings are discussed in light of the relative role that these anxiety-related constructs have in pain and disability, as well as implications for future research.
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Chronic pain and PTSD are known to hold substantial comorbidity following traumatic injury. Although pharmacological agents have been examined in the treatment of pain and PTSD individually, little is known regarding the relationship of medication use with functioning in patients with comorbid conditions. This research examined the relationships of pain, PTSD, and medication use across physical and psychosocial functioning in patients with chronic pain following motor vehicle injury (N=234). ⋯ Opioids also were related to greater psychosocial impairment in patients without PTSD while PTSD was associated with greater impairment in patients not using opioids, (3) Opioid use evidenced a marginal interaction with pain on psychosocial functioning. Opioids were associated with greater psychosocial impairment among patients with high-pain, and high-pain was associated with greater impairment among opioid users, (4) SSRIs held a marginal interaction with PTSD such that PTSD was related to poorer psychosocial functioning only among individuals not using an SSRI, and (5) Anxiolytic use evidenced a marginal interaction with PTSD on physical functioning although no between-group differences were noted. These data suggest that PTSD symptomology may be an important consideration in determining treatment modality for patients experiencing pain subsequent to traumatic injury.
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Patient-controlled analgesia (PCA) has an established role in managing postoperative pain and has been successfully used in-patients with cancer pain. The variation of opioid requirement over a 24h period for patients with cancer pain is debated with suggestions of reduced need over night. ⋯ PCA met individual patient's opioid needs in a safe and effective manner despite a large inter-individual variability in opioid consumption. Moreover, the study indicated a pattern of less opioid requirement at night.
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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.