Pain
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Chronic pain is associated with large societal costs, but few studies have investigated the total costs of chronic pain with respect to elderly subjects. The elderly usually require informal care, care performed by municipalities, and care for chronic diseases, all factors that can result in extensive financial burdens on elderly patients, their families, and the social services provided by the state. This study aims to quantify the societal cost of chronic pain in people of age 65 years and older and to assess the impact of chronic pain on quality of life. ⋯ Consumed resources increased with the severity of chronic pain. Clear differences in EQ-5D were found with respect to the severity of pain. This study found an association between resource use and severity of chronic pain in elderly subjects: the more severe the chronic pain, the more extensive (and expensive) the use of resources.
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The relevance of a phobia-based conceptualization of fear for individuals with chronic pain has been much debated in the literature. This study investigated whether patients with highly fearful chronic low back pain show distinct physiological reaction patterns compared with less fearful patients when anticipating aversive back pain-related movements. We used an idiosyncratic fear induction paradigm and collected 2 different measures of autonomic nervous system activation and muscle tension in the lower back. ⋯ According to Bradley and Lang defense cascade model, this response is typical of a fear reaction. Participants showing the psychophysiological pattern typical of fear also had elevated scores on some self-report measures of components of the fear-avoidance model, relative to participants showing the reaction pattern characteristic of attention. This study is the first to provide psychophysiological evidence for the fear-avoidance model of chronic pain.
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Inflammatory hyperalgesia is a complex process that depends on the sensitization of primary nociceptive neurons triggered by proinflammatory mediators, such as interleukin 1β (IL-1β). Recently, the peripheral activation of caspase-1 (previously known as IL-1β-converting enzyme) was implicated in the induction of acute inflammatory pain by promoting the processing of IL-1β from its precursor form, pro-IL-1β. Caspase-1 activation in several systems requires the assembly of an intracellular molecular platform called an inflammasome. ⋯ The reduced hyperalgesia was accompanied by significant impairments in the levels of mature forms of IL-1β (p17) and caspase-1 (p20) compared to wild-type mice at the inflammatory site. Therefore, these results identified the inflammasome components NLRC4 and ASC as the molecular platform involved in the peripheral activation of caspase-1 and IL-1β maturation, which are responsible for the induction of acute inflammatory pain. In conclusion, our study provides new therapeutic targets for the control of acute inflammatory pain.