Pain
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Randomized Controlled Trial Clinical Trial
Codeine 20 mg increases pain relief from ibuprofen 400 mg after third molar surgery. A repeat-dosing comparison of ibuprofen and an ibuprofen-codeine combination.
A combination of 20 mg codeine base and ibuprofen 400 mg was compared with ibuprofen 400 mg in a randomised double-blind cross-over study of multiple doses in 25 patients after 2-stage bilateral third molar removal. The combination produced significantly greater pain relief and doubled the hours of minimum pain intensity and maximal relief on the day of surgery. ⋯ There was no significant increase in side-effect incidence with the combination. The 30% increase in analgesic effect may be of clinical benefit, and this trial design, cross-over with multiple dosing in out-patients, may be a sensitive test for analgesics, potentially more predictive of side-effect problems than single-dose studies.
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The present study examined catastrophizing in rheumatoid arthritis (RA) patients. Subjects were 223 RA patients who were participants in a longitudinal study. Each patient completed the Catastrophizing scale of the Coping Strategies Questionnaire (CSQ) on 2 occasions separated by 6 months (time 1, time 2). ⋯ Predictive findings regarding catastrophizing while modest were obtained after controlling for initial scores on the dependent variables, demographic variables (age, sex, socioeconomic status), duration of pain, and disability support status. Taken together, these findings suggest that catastrophizing is a maladaptive coping strategy in RA patients. Further research is needed to determine whether cognitive-behavioral interventions designed to decrease catastrophizing can reduce pain and improve the physical and psychological functioning of RA patients.
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Case Reports
An unusual case of causalgia. Relevance to recent hypothesis on mechanism of causalgia.
Intravenous regional sympathetic block with guanethidine caused only limited improvement in a patient with longstanding causalgia. Lumbar sympathetic block with phenol also had little direct effect on the pain but completely abolished associated allodynia and vasomotor signs. ⋯ This improvement persisted even after 8 months when there was some return of the previous allodynia and vasomotor signs (to involve a smaller area than previously). The case would appear to have implications for a recently proposed hypothesis concerning the mechanism of pain in causalgia.
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In the first part of the study 20 subjects (11 headache, 9 normals) free-sorted descriptors from the intensity and affect scales of the Tursky pain perception profile (PPP) into groups on the basis of similar meaning. In part 2 they made similarity ratings of all pairs of words within the intensity and affect scales. In the third part of the study subjects completed a cross-modal matching task to scale the intensity and affect words. ⋯ An MDS analysis showed that the groups could be located in 2-dimensional space in which the dimensions of intensity and affective distress could be easily discerned. When the descriptors from the intensity and affect scales were rated within each scale, a second MDS analysis showed that, whereas the intensity descriptors could be fitted by a 1-dimensional representation, the affect descriptors required a 3-dimensional model. There was evidence that subjects with extensive pain experience placed greater weight on the second and third affective dimensions compared with relatively pain-free subjects.
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Intrathecal administration of glycine (strychnine) or GABA (bicuculline) but not opioid (naloxone), adrenergic (phentolamine) or serotonin (methysergide) receptor antagonists resulted in a dose-dependent organized agitation response to light tactile stimulation. This effect was maximally evoked by oscillating but not continuous stimulation applied to a dermatome corresponding to the levels of spinal cord acted upon by the intrathecal antagonist. Similar results were observed in chloralose-urethane anesthetized rats in which tactile stimulation evoked hypertensive responses following local tactile stimuli. ⋯ At doses below those which produced motor dysfunction, however, these agents had no effects on the hot-plate response latency. These data emphasize that low threshold afferent input is likely subject to an ongoing modulation, the loss of which results in a miscoding of the afferent stimulus yielding a pain relevant message. The lack of effect of agents having a powerful effect on somatic pain stimuli and the converse effects of glutamate receptor antagonists on the strychnine hyperesthesia at doses which do not affect the somatic pain response indicate discriminable processing systems, the characteristics of which resemble the clinical phenomenon observed in patients suffering from sensory dysesthesia following central and peripheral horn injury.