Pain
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We hypothesized that preoperative emotional distress and pain intensity would predict the occurrence of signs and symptoms of complex regional pain syndrome (CRPS) following total knee arthroplasty (TKA). Depression (Beck Depression Inventory, BDI), anxiety (State Trait Anxiety Inventory, STAI), pain (McGill Pain Questionnaire-Short Form, MPQ), and signs/symptoms meeting IASP criteria for CRPS were assessed preoperatively, and at 1-, 3-, and 6-months postoperatively in 77 patients undergoing TKA. The prevalence of subjects fulfilling CRPS criteria was 21.0% at 1 month, 13.0% at 3 months, and 12.7% at 6 months postoperative. ⋯ Post-TKA patients with CRPS were more depressed at 1-month follow-up (P<0.05) and more anxious at 6-month follow-up (P<0.05) than patients with ongoing non-CRPS pain (all other comparisons non-significant, P>0.10). Overall, results indicate that CRPS-like phenomena occur in a significant number of patients early post-TKA; however, it is not associated with significantly greater complaints of postoperative pain. There appears to be a modest utility for preoperative distress and pain in predicting CRPS signs and symptoms following TKA, although false positive rates are relatively high.
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Comparative Study
Genotype-dependence of gabapentin and pregabalin sensitivity: the pharmacogenetic mediation of analgesia is specific to the type of pain being inhibited.
The antiepileptic drug, gabapentin, and another structurally related compound, pregabalin, are increasingly employed in the pharmacotherapy of chronic pain states, although their primary mechanism of action remains a topic of active study. A genomic approach to the study of these drugs may elucidate their potentially novel mechanisms. We examined the heritability of sensitivity to analgesia from gabapentin and pregabalin as a precursor to linkage mapping efforts. ⋯ However, there was virtually no correlation between strain sensitivities to pregabalin inhibition of formalin nociception and zymosan thermal hyperalgesia. In light of previous data from our laboratory and others regarding morphine analgesia, we now establish and empirically demonstrate the general principle that pharmacogenetic mechanisms underlying analgesic sensitivity are specific to the type of pain being inhibited. This has considerable implications for ongoing pharmacogenetic investigations and, more generally, for the choices of preclinical models of pain used in drug development.
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Clinical Trial
Initial pharmacokinetic, safety and efficacy evaluation of nasal morphine gluconate for breakthrough pain in cancer patients.
Patients with controlled background pain associated with cancer frequently also experience episodes of moderate to severe intensity breakthrough pain. Opioid pharmacotherapy, particularly with oral morphine, remains the cornerstone for the management of cancer pain. Nasal administration of opioids provides a mechanism for more rapid drug absorption and more rapid onset of pain relief compared with oral dosing. ⋯ Patient satisfaction ratings were high. These results show that nasal morphine has rapid absorption and apparent onset of effect. Additional multi-dose, dose-ranging and placebo-controlled studies of nasal morphine for cancer pain are warranted.
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The characteristics of spatial summation of pressure pain are not clear. Pressure pain threshold (PPT) and perceived pressure pain intensity were measured in the hand, painfree back and myofascial trigger points (MTPs) in the back, using three different stimulus areas (0.5, 1 and 2 cm(2)). PPT decreased and perceived pain increased significantly with an increase in stimulation area in all the regions (e.g. ⋯ In conclusion, both PPT and perceived pressure pain intensity are subject to a considerable spatial summation in all the regions tested. The quality of pressure-evoked pain is probably determined by this spatial summation. Body region significantly affects the PPT level for a fixed stimulation area but not the magnitude of its spatial summation for areas up to 2 cm(2), which are probably within the receptive field of single spinal nociceptive neurons.
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Comparative Study
Blood pressure but not cortisol mediates stress effects on subsequent pain perception in healthy men and women.
Research has demonstrated that exposure to acute stress may attenuate pain perception. Mechanisms of this effect in humans have not been determined. This study was conducted to determine the extent to which psychophysiological and adrenocortical responses to acute stress predict subsequent pain perception. ⋯ Regression analyses demonstrated that the stress effect on pain ratings was mediated by systolic BP level during stress; however, cortisol responses did not affect this relationship. Mood changes were independent predictors of pain. The study demonstrates that BP changes in response to stress mediate the stress-induced attenuation of pain perception.