Pain
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A transdermal formulation of fentanyl (TTS-fentanyl, Alza Corp., Palo Alto, CA) was evaluated in 13 surgical patients after an abdominal operation. An intraoperative dose of fentanyl (100-200 micrograms i.v.) was administered at the same time as the TTS-fentanyl systems (50-125 micrograms/h) were applied to the antero-lateral chest wall. The TTS-fentanyl systems remained in situ for 24 h and were then removed and a second lot of systems were applied to the contra-lateral chest wall. ⋯ These effects were due to the combined effects of a sustained blood fentanyl concentration and the intermittent supplementary pethidine doses. Side effects due to the topical formulation were transient and included erythema (8 patients) and a minor rash (2 patients) in the area occluded by the systems. The TTS-fentanyl systems provided a significant contribution to postoperative pain control but, at the TTS dose rates used, supplementary doses of pethidine were required by all patients probably to control 'incident' pain.
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Human pain responsivity was defined as the subject's behavioral pain endurance time (PET) to the 1 +/- 0.3 degrees C cold-pressor test, a naturalistic and clinical analogue tonic pain model. Over the past 2 years, we have consistently observed a behavioral dichotomy of pain responsivity in each of our 6 studies (all at P less than 0.000001 effect level), totaling 205 subjects. Overall, the pain-tolerant (PT) subjects could endure the whole 5 min (note that 3 min was the ceiling criterion in the last study) of cold-pressor test, while the pain-sensitive (PS) subjects could merely tolerate the test for an overall mean of 60 sec, 20% of PET in the PT group. ⋯ The psychological/physiological etiology of such drastic human pain responsivity requires intense systematic investigations. This report discusses the results in: (a) individual differences in pain responsivity, (b) characterization of the cold-pressor test as a model for tonic pain, (c) contrast between PS and PT groups of pain perception and state anxiety, and (d) psychological determinants of measures for cognitive, perceptual and affective domains. Discussion was also focused on the experimental tonic pain model and its generality for clinical pain, as well as the basic model of the cold-pressor test for human tonic pain responsivity.
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Fifty-six consecutive patients with pain due to cancer were admitted to a prospective study designed to test a clinical staging system for cancer pain. The system classifies patients in stage 1 (good prognosis) to stage 3 (poor prognosis) according to the mechanism of pain, characteristics of pain, previous narcotic exposure, cognitive function, psychological distress, tolerance and past history of drug addiction or alcoholism. During day 1 patients were staged after being seen by one of the investigators. ⋯ Eighteen of 22 patients in stage 1 achieved good pain control (82%) vs. 2/22 patients in stage 3 (10%; P less than 0.01). Sensitivity, specificity and negative predictive value of the system were 0.75, 0.86 and 0.80, respectively. We conclude that this is a simple and reliable system for clinical staging that can be used for clinical research and management of patients with cancer pain.
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Case Reports Comparative Study
Central post-stroke pain--a study of the mechanisms through analyses of the sensory abnormalities.
The somatosensory abnormalities in 20 men and 7 women (mean age 67 years, range 53-81) with central post-stroke pain (CPSP) have been analysed in detail with traditional neurological tests and quantitative methods. The cerebrovascular lesions were located in the lower brain-stem in 8 patients, involved the thalamus in 9 and in 6 were suprathalamic. In 4 patients the location of the CVL could not be determined. ⋯ The results indicate that all patients with CPSP have lesions that affect the major pathways for temperature and pain sensibility, i.e., the spino-thalamo-cortical pathways. Furthermore it appears that neither the level of the lesion along the neuraxis nor concomitant injury to the medial lemniscal pathways is crucial for the development of CPSP. The results confirm the notion that CPSP is a deafferentation syndrome, but they also provide evidence against the hypothesis that CPSP is a release phenomenon caused by a lesion that removes inhibitory influences of the lemniscal pathways on neurones that evoke pain.
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Individual differences in human pain responsivity were characterized by the 1 degree C cold-pressor test. Behaviorally, a pain-tolerant group (PT = 29 Ss) tolerated the entire 3-min test (means = 180 +/- 0 sec), while a pain-sensitive group (PS = 13 Ss) averaged only 50.31 +/- 20.81 sec of the cold-pressor test (t = 16.75, P less than 0.0001), replicating our earlier studies. ⋯ However, the PS subjects showed significantly higher delta power, but not beta power, than the PT subjects. We conclude that heightened delta activity may reflect the stress component of human pain responsivity, and that beta activity reflects the vigilance scanning of pain processes.