Pain
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Results from laboratory and naturalistic studies have demonstrated decreased subjective pain ratings in hypertensives and individuals at risk for hypertension. Based on previous evidence that the nociceptive withdrawal reflex may provide an objective index of pain threshold in humans, the present study examined the intensity of sural nerve stimulation required to elicit nociceptive withdrawal in offspring of hypertensives and normotensives. Participants included 60 men and 56 women who were normotensive, 18-23 years of age, and predominately Caucasian. ⋯ Second, offspring of hypertensives endured significantly more intense stimulation before reporting pain. Third, both parental history of hypertension and resting systolic blood pressure were significant independent predictors of stimulation intensity at nociceptive withdrawal reflex and subjective pain thresholds. These results confirm and extend previous observations of an association between risk for hypertension and hypoalgesia, and suggest that hypoalgesia should be examined as a potential predictor of progressive blood pressure increases in individuals at risk for hypertension.
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Our previous studies in the Sprague-Dawley rat showed that the intrinsic antinociceptive effects of oxycodone are naloxone reversible in a manner analogous to morphine but that in contrast to morphine, oxycodone's antinociceptive effects have a rapid onset of maximum effect (approximately 5-7 min compared to 30-45 min for morphine), comprise one antinociceptive phase (compared to two phases) and are of relatively short duration (approximately 90 min compared to approximately 180 min). In the present study, administration of a range of selective opioid receptor antagonists has shown that the intrinsic antinociceptive effects of oxycodone (171 nmol) are not attenuated by i.c.v. administration of (i) naloxonazine, a mu1-selective opioid receptor antagonist, or (ii) naltrindole, a delta-selective opioid receptor antagonist, in doses that completely attenuated the intrinsic antinociceptive effects of equipotent doses of the respective mu- and delta-opioid agonists, morphine and enkephalin-[D-Pen(2,5)] (DPDPE). ⋯ Importantly, the antinociceptive effects of oxycodone (171 nmol i.c.v.) were markedly attenuated by the prior i.c.v. administration of the selective kappa-opioid receptor antagonist, norbinaltorphimine (nor-BNI), in a dose (0.3 nmol) that did not attenuate the antinociceptive effects of an equipotent dose of i.c.v. morphine (78 nmol). Taken together, these data strongly suggest that the intrinsic antinociceptive effects of oxycodone are mediated by kappa-opioid receptors, in contrast to morphine which interacts primarily with mu-opioid receptors.
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Comparative Study Clinical Trial Controlled Clinical Trial
Pain coping strategies that predict patients' and spouses' ratings of patients' self-efficacy.
This study examined the relationship of pain coping strategies to osteoarthritis patients' ratings of self-efficacy and to spouses' ratings of the patients' self-efficacy. Subjects, 130 individuals having osteoarthritis of the knees and persistent knee pain, completed a pain coping strategies measure (the Coping Strategies Questionnaire), a measure of self-efficacy (the Arthritis Self-Efficacy Scale), and a measure of pain (the McGill Pain Questionnaire). Two sets of regression analyses were conducted, one examining the degree to which pain coping strategies predicted patients' self-efficacy ratings, and the other examining the degree to which coping strategies predicted spouses' ratings of the patients' self-efficacy. ⋯ The findings regarding coping strategies were particularly interesting in that they were obtained even after controlling for pain intensity and demographic variables. The pain coping strategies identified are potentially important targets for cognitive-behavioral assessment and treatment efforts. Interventions designed to increase the use of adaptive pain coping strategies and decrease the use of maladaptive pain coping strategies could enhance self-efficacy, reduce pain, and improve the physical and psychological functioning of individuals having osteoarthritis.
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Clinical Trial Controlled Clinical Trial
Afferent large fiber polyneuropathy predicts the development of postherpetic neuralgia.
Acute zoster infection may be followed by a chronic pain syndrome, i.e., postherpetic neuralgia (PHN). Besides older age, the intensity of pain and neuronal damage within the acutely affected body region are regarded as predictors or risk factors for PHN. As an alternative approach an underlying peripheral polyneuropathy may be considered as potential co-factor. ⋯ Nociceptive C-fiber and parasympathetic fiber function demonstrated no significant differences in both groups. Acute zoster pain was slightly more intense in the PHN group. We concluded that (i) a mild generalized impairment of afferent A beta-fiber function (A beta-polyneuropathy) seems to be an important co-factor in the development of PHN and (ii) impairment of vibration sense, i.e., impairment of afferent A beta-fiber function, may be used as a predictor of PHN.
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The purpose of this review was to identify and analyze the controlled clinical trial data for peripheral neuropathic pain (PNP) and complex regional pain syndromes (CRPS). A total of 72 articles were found, which included 92 controlled drug trials using 48 different treatments. The methods of these studies were critically reviewed and the results summarized and compared. ⋯ The methods scores were higher (P < 0.01) for the PNP trials (66.2 +/- 1.5, n = 66) than the CRPS trials (57.6 +/- 2.9, n = 26). The CRPS trials tended to use less subjects and were less likely to use placebo controls, double-blinding, or perform statistical tests for differences in outcome measures between groups. There was almost no overlap in the controlled trial literature between treatments for PNP and CRPS, and treatments used in both conditions (intravenous phentolamine and epidural clonidine) had similar results.