Pain
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Age differences in the experience of chronic pain remain unclear. A serious barrier to progress in the field of pain and aging arises from the lack of data regarding the psychometric properties of pain scales for use with the elderly. The present study was designed to assess age differences in pain intensity and quality and to compare the psychometric properties of the McGill Pain Questionnaire (MPQ) in young and elderly chronic pain patients. ⋯ Finally, the latent structure, internal consistency, and pattern of subscale correlations of the MPQ were very similar in the young and elderly groups. Possible explanations for the discrepancy in the pattern of age differences on measures of pain intensity and quality are explored. The implications of this pattern of age differences for basic pain mechanisms and pain management should be given serious empirical attention.
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Randomized Controlled Trial Comparative Study Clinical Trial
Different lipid profiles as constituencies of liquid formula diets do not influence pain perception and the efficacy of opioids in a human model of acute pain and hyperalgesia.
Nutritional support and pain control by medication are often used concomitantly, but interactions are hardly investigated. A randomised, double-blind, cross-over study in ten right-handed volunteers was performed evaluating the influence of cholecystokinin (CCK)-excretion on the perception of pain in a standardised model. CCK-excretion was induced by a liquid formula diet with either long- or medium-chain triglycerides (LCT, MCT). ⋯ In a second series of experiments, alfentanil (4.1+/-0.5 mg) was administered for 90 min using target-controlled infusions and measurements were performed as stated above. Oral administration of LCT as well as MCT may lead to different CCK blood levels, but we found no evidence for CCK-induced effects on pain sensation, touch-evoked allodynia, secondary hyperalgesia or morphine-induced anti-nociception in humans. In our studies, liquid formula diets did not influence acute pain perception or the efficacy of opioids in a human model of pain.
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Randomized Controlled Trial Comparative Study Clinical Trial
Negative affect: effects on an evaluative measure of human pain.
Prior work indicates that exposure to fear-inducing shock inhibits finger-withdrawal to radiant heat in humans (hypoalgesia), whereas anxiety induced by threat of shock enhances reactivity (hyperalgesia; Pain 84 (2000) 65-75). Although finger-withdrawal latencies are thought to reflect changes in pain sensitivity, additional measures of pain are needed to determine whether pain perception is altered. The present study examined the impact of negative affect on visual analog scale (VAS) ratings of fixed duration thermal stimuli. ⋯ Results suggest that both negative affect manipulations reduced pain. Manipulation checks indicated that the emotion-induction treatments induced similar levels of fear but with different arousal levels. Potential mechanisms for affect induced changes in pain are discussed.
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Comparative Study
Differential effects of expressive anger regulation on chronic pain intensity in CRPS and non-CRPS limb pain patients.
Research has shown that the anger management styles of both anger-in (suppression of anger) and anger-out (direct verbal or physical expression of anger) may be associated with elevated chronic pain intensity. Only the effects of anger-out appear to be mediated by increased physiological stress responsiveness. Given the catecholamine-sensitive nature of pain mechanisms in complex regional pain syndrome (CRPS), it was hypothesized that anger-out, but not anger-in, would demonstrate a stronger relationship with chronic pain intensity in CRPS patients than in non-CRPS chronic pain patients. ⋯ The AIS main effect on MPQ-A ratings was accounted for entirely by overlap with negative affect. Results are consistent with a greater negative impact of anger-out on chronic pain intensity in conditions reflecting catecholamine-sensitive pain mechanisms, presumably due to the association between anger-out and elevated physiological stress responsiveness. These results further support previous suggestions that anger-in and anger-out may affect pain through different mechanisms.
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Hypersensitivity to a variety of sensory stimuli is a feature of persistent whiplash associated disorders (WAD). However, little is known about sensory disturbances from the time of injury until transition to either recovery or symptom persistence. Quantitative sensory testing (pressure and thermal pain thresholds, the brachial plexus provocation test), the sympathetic vasoconstrictor reflex and psychological distress (GHQ-28) were prospectively measured in 76 whiplash subjects within 1 month of injury and then 2, 3 and 6 months post-injury. ⋯ The differences in GHQ-28 did not impact on any of the sensory measures. These findings suggest that those with persistent moderate/severe symptoms at 6 months display, soon after injury, generalised hypersensitivity suggestive of changes in central pain processing mechanisms. This phenomenon did not occur in those who recover or those with persistent mild symptoms.