Pain
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Previous research has demonstrated a relationship between cognitive pain coping activity and adjustment in pain patients. The empirically derived dimensions of coping activity, as measured by scales from the Coping Strategy Questionnaire (CSQ), however, have varied across investigations. The purpose of this investigation was to determine both the content and number of dimensions of the CSQ and to explore the potential moderating influence that sociodemographic and patient history variables may have on the latent structure of the CSQ. ⋯ A third factor, which was somewhat less stable, appeared to reflect avoidance of pain by attention to non-pain-related mental activity (with high loadings on diverting attention and praying and hoping). Scales reflecting catastrophizing cognitions and behavioral coping strategies did not consistently load on the above dimensions. Issues concerning the conceptualization and measurement of pain-related cognitive coping dimensions are discussed.
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Comparative Study
Comparison of the effects of ureteral calculosis and occlusion on muscular sensitivity to painful stimulation in rats.
An animal model of muscular hyperalgesia was developed. In humans, this disorder follows painful crises due to ureteral calculosis. Changes in vocalization thresholds to electrical stimulation of the obliquus externus muscle of both sides were studied in a group of rats with chronically implanted muscles before and after the production of a stone in one ureter. ⋯ Ligature alone never induced any hyperalgesic effect. Stone plus ligature produced a marked hyperalgesia (max 39%) in the ipsilateral muscle, which lasted for only 5 days. It is concluded that the ureteral stone is the factor responsible for the appearance of muscular hyperalgesia.
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Partial nerve injury is the main cause of causalgiform pain disorders in humans. We present here a novel animal model of this condition. In rats we unilaterally ligated about half of the sciatic nerve high in the thigh. ⋯ Pin-prick evoked such exaggerated responses bilaterally (mechanical hyperalgesia). In a companion report, we show that these abnormalities critically depend on the sympathetic outflow. Based on the immediate onset and long-lasting perpetuation of similar symptoms, such as touch-evoked allodynia and hyperalgesia, and the resemblance of the contralateral phenomena to 'mirror image' pains in some humans with causalgia, we suggest that this preparation may serve as a model for syndromes of the causalgiform variety that are triggered by partial nerve injury and maintained by sympathetic activity.
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Comparative Study
Profiles of opioid analgesia in humans after intravenous bolus administration: alfentanil, fentanyl and morphine compared on experimental pain.
This report examines the relationship of plasma drug concentration to analgesic effect following bolus doses of alfentanil, fentanyl and morphine and assesses individual differences in analgesic response among volunteers. We predicted that the 3 opioids would yield disparate analgesic profiles because their physicochemical and pharmacokinetic characteristics differ. Ten healthy volunteers received intravenous bolus doses of either alfentanil, fentanyl, morphine or normal saline on different days. ⋯ Fentanyl exhibited a marked hysteresis. We observed noteworthy individual differences in analgesic response with all 3 drugs but these differences were greatest for morphine and least for alfentanil. Inter- and intrasubject variability in analgesic response across drugs is related to the physicochemical properties of the drugs tested.
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Both conditioning and expectancy models have been offered in recent years as explanations for the placebo response. Following our earlier work on conditioning placebo responses in human subjects the current study examined the relative contribution made by conditioning and verbal expectancy. ⋯ Subjects' responses were compared with and without a placebo cream, using iontophoretic pain stimulation. The results suggest that conditioning was more powerful than verbal expectancy in creating a placebo response.