Pain
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Pain is common in adult life, and the extent to which pain interferes with daily activities rises with age. Little is known about the social factors associated with disabling pain. The objective was to determine the individual and neighbourhood social factors that predict pain that interferes with daily activities. ⋯ Whilst the onset of pain which disrupts daily life is influenced mainly by the characteristics of the pain and by the psychological factors, there are links with the social factors, particularly individual measures of perceived income adequacy. The onset of disabling pain is also influenced by the place where one lives. Policies to prevent disabling pain need to consider the contribution of neighbourhood deprivation and income inequalities to the extent of the problem.
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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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When faced with the problem of pain one can attempt a solution aimed at relief (assimilation) or a solution aimed at acceptance (accommodation). Using this dual process model of adaptation to pain, this study compares acute and chronic pain patients on their approach to problem solving. Three hundred and sixty-four patients were recruited from clinical settings, 303 with chronic pain and 61 with acute pain, and completed a range of measures of both affect and pain-related behavior, including the Pain Solutions Questionnaire. ⋯ Only in the case of catastrophic thinking about pain was it found that the effects of assimilative coping were moderated by pain duration. For chronic pain patients, catastrophic thinking about pain was greater when assimilative coping was higher. These results are discussed within the context of a goal directed motivational model of adaptation to chronic pain.
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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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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.