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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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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Attenuation of the lower limb nociceptive flexion reflex (NFR) during the cardiac cycle has been attributed to inhibition of sensorimotor function by arterial baroreceptor activation. It has been proposed that cardiopulmonary baroreceptors might have similar inhibitory effects. ⋯ Nociceptive responding and pain ratings did not differ between postures suggesting no cardiopulmonary effects. This phasic modulation of the upper limb withdrawal response provides further support for arterial baroreceptor-mediated inhibition of nociceptive transmission.
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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.
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The acid sensing ion channel 3 (ASIC3) is critical for the development of secondary hyperalgesia as measured by mechanical stimulation of the paw following muscle insult. We designed experiments to test whether ASIC3 was necessary for the development of both primary and secondary mechanical hyperalgesia that develops after joint inflammation. We used ASIC3 -/- mice and examined the primary (response to tweezers) and secondary hyperalgesia (von-Frey filaments) that develops after joint inflammation comparing to ASIC3 +/+ mice. ⋯ ASIC3 was found, however, in synoviocytes of the knee joint of uninflamed mice. In ASIC3 +/+ mice with joint inflammation, ASIC3 co-localized with PGP 9.5 or CGRP in joint afferents innervating the synovium. We conclude that the decreased pH that occurs after inflammation would activate ASIC3 on primary afferent fibers innervating the knee joint, increasing the input to the spinal cord resulting in central sensitization manifested behaviorally as secondary hyperalgesia of the paw.