Pain
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The purpose of this study was to verify the usefulness of an adaptation of the stress process model in organizing the psychological variables associated with the development of low-back-pain related disability. French-speaking Canadian workers on compensated sick leave (N=439) due to recent occupational low back pain (LBP) were evaluated during the sub-acute stage of LBP (between 30 and 83 days after injury). They were assessed for the following factors: life events, injury-specific cognitive appraisal, emotional distress, avoidance coping, and functional disability. ⋯ The stress model tested here reaffirms the importance of life events in the development of disability through the more established emotional distress factor. Also, cognitive appraisal appears to have an indirect effect on disability through activity avoidance and distress. This adaptation of the stress model makes it possible to integrate risk factors into a reduced set of meaningful factors and proposes a more general adaptation explanation of disability than the specific fear-avoidance model.
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Painful hypersensitivity to norepinephrine (NE) has been reported in various chronic pain conditions that exhibit sympathetically-maintained pain (SMP), particularly CRPS-I and II. We investigated the parallels between the nociceptive and vascular sensitivity to NE in rats with chronic post-ischemia pain (CPIP), an animal model of CRPS-I induced by hind paw ischemia-reperfusion injury. Intradermal injections of NE to the affected hind paw induced dose-dependent nociceptive behaviours in CPIP rats, but not sham animals. ⋯ These results suggest CPIP rats display abnormal nociceptive responses to adrenergic and non-adrenergic vasoconstrictive agents. Furthermore, the nociceptive responses to NE in CPIP rats are paralleled by enhanced vasoconstrictive responses to NE, and are relieved by alpha-adrenergic antagonists or a vasodilator. We conclude that persistent tissue ischemia and hypersensitivity to sympathetic vasoconstriction are important mechanisms for pain in CPIP rats, and that either reducing vasoconstriction or enhancing vasodilatation may be effective methods of relieving the pain of CRPS-I.
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The development and maintenance of chronic pain are influenced by its social context, and especially by the responses of family members. For children, very few instruments are available that measure pain-related parental behavior. Using the Multidimensional Pain Inventory for adults (MPI; [Kerns RD, Turk DC, Rudy TE. ⋯ Child-perceived maternal behavior was significantly related to overall parenting and to mothers' actual behavior as observed during a cold pressor test. Finally, the PPBI was sensitive to differences in mothers' responses depending on the specific nature of the child's pain. Child and parent reports of parental behaviors were modestly correlated and were differentially related to the validity measures, hence supporting the importance of assessing the social context of pediatric pain independently of both the child's and the parent's perspectives.
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Trying to control pain is a common human goal. But little is know about what happens when one loses control over pain. This paper reports an experiment with 74 healthy volunteers, half of whom were given control over a pain stimulus and subsequently lost control, and half of whom never had control over the pain. ⋯ These findings are discussed within the context of a dual process model of coping with uncontrollable adverse events [Brandtstädter J, Renner G. Tenacious goal pursuit and flexible goal adjustment: explication and age-related analysis of assimilative and accommodative strategies of coping. Psychol Aging 1990;5:58-67] and possible mechanisms for perseverance with ineffective solutions.
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We evaluated the effect of low doses of systemically administered tetrodotoxin (TTX) on the development and expression of neuropathic pain induced by paclitaxel in mice. Treatment with paclitaxel (2mg/kg, i.p., once daily during 5 days) produced long-lasting (2-4 weeks) heat hyperalgesia (plantar test), mechanical allodynia (electronic Von Frey test) and cold allodynia (acetone drop method), with maximum effects observed on days 7, 10 and 10-14, respectively. Acute subcutaneous treatment with 1 or 3 microg/kg of TTX reduced the expression of mechanical allodynia, whereas higher doses (3 or 6 microg/kg) were required to reduce the expression of cold allodynia and heat hyperalgesia. ⋯ Coadministration of a lower dose of TTX (3 microg/kg) also prevented the development of mechanical allodynia. No signs of TTX-induced toxicity or motor incoordination were observed. These data suggest that low doses of TTX can be useful to prevent and treat paclitaxel-induced neuropathic pain, and that TTX-sensitive subtypes of sodium channels play a role in the pathogenesis of chemotherapy-induced neuropathic pain.