Pain
-
Randomized Controlled Trial Comparative Study Clinical Trial
The placebo needle, is it a valid and convincing placebo for use in acupuncture trials? A randomised, single-blind, cross-over pilot trial.
The issue of what constitutes an effective and realistic acupuncture placebo control has been a continuing problem for acupuncture research. In order to provide an effective placebo, the control procedure must be convincing, visible and should mimic, in all respects, apart from a physiological effect, the real active treatment. The 'Streitberger' needle might fulfil these criteria and this paper reports on a validation study. ⋯ No major differences in outcome between real and placebo needling could be found. The fact that nearly 40% of subjects did not find that the two interventions were similar, however, raises some concerns with regard to the wholesale adoption of this instrument as a standard acupuncture placebo. Further work on inter-tester reliability and standardisation of technique is highly recommended before we can be confident about using this needle in further studies.
-
Randomized Controlled Trial Comparative Study Clinical Trial
The association between anger expression and chronic pain intensity: evidence for partial mediation by endogenous opioid dysfunction.
Recent work suggests that an expressive anger management style (anger-out) is associated with elevated acute pain sensitivity due to endogenous opioid antinociceptive dysfunction. We tested the hypothesis that this opioid dysfunction mediates the previously reported positive association between anger-out and chronic pain intensity. To assess endogenous opioid antinociception in the laboratory, 71 subjects with chronic low back pain received opioid blockade (8 mg naloxone i.v.) or placebo in counterbalanced order in separate sessions. ⋯ Inclusion of blockade effects in the first step of the regression resulted in a decrease from 7 to 3% in chronic pain variance accounted for by anger-out. Opioid dysfunction did not mediate the positive association between anger-in and chronic pain. These results provide preliminary support for the hypothesis that the positive association between anger expression and chronic pain intensity is mediated by opioid antinociceptive system dysfunction.
-
Cancer-induced bone pain is a major clinical problem. A rat model based on intra-tibial injection of MRMT-1 mammary tumour cells was used to mimic progressive cancer-induced bone pain. At the time of stable behavioural changes (decreased thresholds to mechanical and cold stimuli) and bone destruction, in vivo electrophysiology was used to characterize natural (mechanical, thermal, and cold) and electrical-evoked responses of superficial and deep dorsal horn neurones in halothane-anaesthetized rats. ⋯ Deep WDR neurones showed less pronounced changes to the superficial dorsal horn, however, the response to thermal and electrical stimuli, but not mechanical, were significantly increased in the MRMT-1-injected rats. In conclusion, the spinal cord is significantly hyperexcitable with previously superficial NS cells becoming responsive to wide-dynamic range stimuli possibly driving this plasticity via ascending and descending facilitatory pathways. The alterations in superficial dorsal horn neurones have not been reported in neuropathy or inflammation adding to the evidence for cancer-induced bone pain reflecting a unique pain state.
-
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.
-
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.