Pain
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Clinical Trial Controlled Clinical Trial
Independent effects of ischaemia and noradrenaline on thermal hyperalgesia in capsaicin-treated skin.
Noradrenaline increases thermal hyperalgesia in skin previously sensitized by capsaicin. The aim of the present study was to determine whether a vasoconstrictor ischaemic effect of noradrenaline increases thermal hyperalgesia. Heat pain thresholds were measured in the capsaicin-treated and untreated skin on the forearms of 13 normal volunteers. ⋯ Thermal hyperalgesia subsided in control sites in the capsaicin-treated skin after cuff pressure was released, but persisted at sites of noradrenaline iontophoresis (in the capsaicin-treated skin, mean heat pain threshold during reactive hyperaemia 45.2 +/- 5.1 degrees C at the noradrenaline site compared with 49.3 +/- 6.0 degrees C at control sites, P < 0.01; in the untreated skin, mean heat pain threshold at the noradrenaline site 46.5 +/- 3.3 degrees C compared with 48.8 +/- 3.0 degrees C at control sites, P < 0.001). Arterial occlusion could increase thermal hyperalgesia in capsaicin-treated skin by preventing the dispersal of nociceptive substances peripherally or through central summation of nociceptive signals. The hyperalgesic effect of noradrenaline is greater than the hyperalgesic effect of ischaemia, suggesting that some mechanism in addition to vasoconstriction contributes to the nociceptive effect of noradrenaline.
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This study examined the relative predictive validities of several measures of pain intensity. Forty chronic pain patients completed 6-14 days worth of hourly pain ratings, which were averaged to obtain a measure of actual average pain intensity. These patients then made ratings, on 101-point numerical rating scales, of worst, least, and usual pain during the previous 2 wks, and of their current pain. ⋯ Of all possible composites of usual, least, worst, and current pain ratings, the arithmetic mean of least and usual pain had the strongest relationship to actual average pain. The inclusion of ratings of most pain or current pain in any composite score actually weakened the relationship between the composite score and actual average pain intensity. These results suggest that, when clinicians or researchers wish to assess average pain among chronic pain patients, but cannot obtain multiple measures of pain over time, the most valid measure would be the arithmetic mean of patient-recalled least and usual pain.
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In the present study, Brandtstädter's (1992) distinction between assimilation and accommodation as two fundamental means of coping is applied to the field of chronic pain. Assimilative coping involves active attempts (e.g. instrumental activities, self-corrective actions, compensatory measures) to alter unsatisfactory life circumstances and situational constraints in accordance with personal preferences. Conversely, accommodative coping (e.g. downgrading of aspirations, positive reappraisal, self-enhancing comparisons) is directed towards a revision of self-evaluative and personal goal standards in accordance with perceived deficits and losses. ⋯ Most important, the ability to flexibly adjust personal goals attenuated the negative impact of the pain experience (pain intensity, pain-related disability) on psychological well-being (depression). Furthermore, pain-related coping strategies led to a reduction of disability only when accompanied by a high degree of flexible goal adjustment. The theoretical and clinical implications of these findings for coping research and the treatment of chronic pain patients are discussed.
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N-Methyl-D-aspartate (NMDA) receptor antagonists have been repeatedly shown to attenuate the development of opiate tolerance and dependence in rodents. In the present experiments, continuous subcutaneous infusion of either MK-801 (0.01 mg/kg/h but not 0.005 mg/kg/h) or DM (0.133, 0.67 and 1.33 mg/kg/h) reliably prolonged the antinociceptive effect of continuous subcutaneous infusion of morphine sulfate (2.0 mg/kg/h), indicating attenuation of the development of morphine tolerance. Furthermore, this prolonged antinociception was completely reversible by naloxone (10 mg/kg, i.p.). ⋯ The effects of MK-801 on all withdrawal symptoms were confounded, however, by the appearance of flaccidity following naloxone administration to rats having received MK-801 and morphine. These results extend previous observations by showing that the prolonged antinociception observed following co-administration of morphine and an NMDA antagonist is completely naloxone-reversible, supporting the notion that this antinociception reflects prolongation of an opioid receptor-mediated effect. The different profiles of side effects associated with MK-801 and DM, however, suggest that (1) attenuation of naloxone-precipitated withdrawal symptoms by MK-801 may be an artifact of toxicity, and (2) DM may prove clinically useful for the prevention of morphine tolerance, given its lack of observable side effects when administered concurrently with morphine to rodents.
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Two established phenomena contribute to the generation of post-injury pain hypersensitivity: peripheral sensitization, an increase in transduction sensitivity of high threshold A delta and C-fibre nociceptors, and central sensitization, an increase in excitability of neurones in the spinal cord triggered exclusively by C-fibre inputs. We now describe a novel phenomenon: progressive tactile hypersensitivity, which contributes to a cumulative allodynia during inflammation. Behavioural measurements in conscious intact animals showed that repeated light touch stimuli delivered at 5-min intervals to an inflamed paw, established 48 h earlier by an intra-plantar injection of complete Freund's adjuvant (CFA), resulted in a progressive reduction in the mechanical withdrawal threshold by more than 75%, from its already hypersensitive basal level. ⋯ Progressive hypersensitivity, measured here as a progressive tactile allodynia after inflammation in either intact or decerebrate-spinal rats, with its gradual build-up and contribution from A beta fibres, is very different from the central sensitization induced by C-fibre stimulation which is characterised by a peak increase in excitability soon after the conditioning input followed by a steady decrement to baseline levels. Progressive hypersensitivity is likely to be the consequence of an alteration in the function and phenotype of afferents innervating inflamed tissue and the pattern of excitation they produce in spinal neurones. The phenomenon may have an important role in the development of inflammatory pain and hypersensitivity.