Pain
-
Many people with hemophilia are affected by chronic arthritic joint pain as well as acute bleeding pain. In this cross-sectional study, 209 men with hemophilia A or B completed the Hemophilia Pain Coping Questionnaire (HPCQ), the Chronic Pain Acceptance Questionnaire (CPAQ), and the RAND 36-item Health Survey (SF-36), a measure of health-related quality of life. Multiple regression was used to test the influence of active pain coping, passive adherence coping, and negative thoughts about pain (HPCQ scales), and activity engagement and pain willingness (CPAQ scales), on physical and mental components of quality of life (SF-36 PCS and MCS scales), taking account of age, hemophilia severity, use of clotting factor, and pain intensity. ⋯ Negative thoughts moderated and partly mediated the influence of pain intensity on mental quality of life. There was no evidence that active pain coping influenced quality of life. The findings suggest that quality of life in hemophilia could potentially be improved by interventions to increase pain acceptance and reduce negative thoughts about pain.
-
Earlier, we showed that streptozocin (STZ)-induced type 1 diabetes in rats leads to the development of painful peripheral diabetic neuropathy (PDN) manifested as thermal hyperalgesia and mechanical allodynia accompanied by significant enhancement of T-type calcium currents (T-currents) and cellular excitability in medium-sized dorsal root ganglion (DRG) neurons. Here, we studied the in vivo and in vitro effects of gene-silencing therapy specific for the Ca(V)3.2 isoform of T-channels, on thermal and mechanical hypersensitivities, and T-current expression in small- and medium-sized DRG neurons of STZ-treated rats. ⋯ Furthermore, treatments of diabetic rats with daily insulin injections reversed T-current alterations in DRG neurons in parallel with reversal of thermal and mechanical hypersensitivities in vivo. This confirms that Ca(V)3.2 T-channels, important signal amplifiers in peripheral sensory neurons, may contribute to the cellular hyperexcitability that ultimately leads to the development of painful PDN.
-
Comparative Study
Gender role expectations of pain is associated with pain tolerance limit but not with pain threshold.
Gender role expectations of pain (GREP) was suggested to predict sex differences in pain perception. Our aim was to explore sex differences in GREP and investigate its relationship with heat-pain threshold (HPT) and heat-pain tolerance limit (HPTL). University students (115 males, 134 females) filled the GREP questionnaire. ⋯ Both males and females held stereotypical "macho" attitude towards themselves with regard to pain sensitivity and willingness to report of pain however only females held stereotypical, "macho" attitude towards themselves with regard to pain endurance. The sex differences in GREP and in HPTL and the correlations between GREP items and experimental thresholds suggest that the relationship between GREP and experimental pain is complex and sex-specific. It also appears that GREP is affected by culture.
-
In healthy adults, expectations can modulate the activity of inhibitory bulbo-spinal projections, and can even block the analgesic properties of counter-irritation - a phenomenon that triggers descending inhibition. Since descending inhibition is known to be deficient in fibromyalgia (FM) patients, we tested the possibility that expectancy-mediated analgesia would improve, or even kick-start, the deficient inhibitory responses of FM patients. By measuring subjective pain ratings, spinal withdrawal reflexes, and somatosensory evoked potentials (SEP), it was possible to test whether or not expectancy-mediated analgesia involved descending inhibition in FM patients. ⋯ However, even when analgesia was experienced, the spinal activity of FM patients was abnormal, showing heightened reflex responses. This demonstrates that, unlike healthy subjects, the modulation of pain by expectations in FM fails to influence spinal activity. These results indicate that FMs are capable of expectancy-induced analgesia but that, for them, this form of analgesia does not depend on the recruitment of descending inhibitory projections.
-
The neural mechanisms whereby placebo conditioning leads to placebo analgesia remain unclear. In this study we aimed to identify the brain structures activated during placebo conditioning and subsequent placebo analgesia. We induced placebo analgesia by associating a sham treatment with pain reduction and used fMRI to measure brain activity associated with three stages of the placebo response: before, during and after the sham treatment, while participants anticipated and experienced brief laser pain. ⋯ However, during altered pain experience only aMCC, post-central gyrus and posterior cingulate demonstrated altered activity. The common frontal cortical areas modulated during anticipation in both the placebo conditioning and placebo analgesia phases have previously been implicated in placebo analgesia. Our results suggest that the main effect of placebo arises from the reduction of anticipation of pain during placebo conditioning that is subsequently maintained during placebo analgesia.