Pain
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In the past 30years, the study of nociception has relied mostly on thermal stimulation to activate nociceptors selectively. However, thermal stimulation suffers from some important limitations. For this reason, investigators have proposed intra-epidermal electrical stimulation (IES) as an alternative method to activate nociceptors selectively. ⋯ In a second experiment, we applied a nerve pressure block to the superficial radial nerve to induce a temporally dissociated impairment of Abeta-, Adelta- and C-fibre afferents, and thereby determine the fibre populations contributing to the responses elicited by IES. We found that the time course of the blockade of the responses to IES follows closely the time course of the blockade of Adelta-fibres, but not of Abeta-fibres. Taken together, our results provide converging evidence that Adelta-nociceptors can be activated selectively using IES, provided that low intensities of stimulation are used.
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Hydrogen sulfide (H(2)S) formed from l-cysteine by multiple enzymes including cystathionine-gamma-lyase (CSE) is now considered a gasotransmitter in the mammalian body. Our previous studies have shown that H(2)S activates/sensitizes Ca(v)3.2 T-type Ca(2+) channels, leading to facilitation of somatic and visceral nociception, and that CSE-derived endogenous H(2)S participates in inflammatory pain. Here, we show novel evidence for involvement of the endogenous H(2)S-Ca(v)3.2 pathway in neuropathic pain. ⋯ Finally, silencing of Ca(v)3.2 in DRG by repeated intrathecal administration of Ca(v)3.2-targeting siRNA significantly attenuated the neuropathic hyperalgesia in the L5SNC rat. In conclusion, our data suggest that Ca(v)3.2 T-type Ca(2+) channels in sensory neurons are upregulated and activated/sensitized by CSE-derived endogenous H(2)S after spinal nerve injury, contributing to the maintenance of neuropathic pain. We thus propose that Ca(v)3.2 and CSE could be targets for the development of therapeutic drugs for the treatment of neuropathic pain.
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This study supports the hypothesis that healthy older adults exhibit decreased endogenous pain inhibition compared to younger healthy controls. Twenty-two older adults (56-77years of age) and 27 controls aged 20-49 participated in five experimental sessions following a training session. Each experimental session consisted of five 60-s trials in which the experimental heat stimulus was presented to the thenar eminence of the left palm with or without a conditioning stimulus (cold-water immersion of the foot). ⋯ A novel aspect of the study was that we recorded "pain offset" (i.e., after-sensations) and found that ratings for the older sample decreased at a slower rate than observed for the group of younger adults suggesting increased central sensitization among the older sample. Decrements in CPM could contribute to the greater prevalence of pain in older age. Since a number of neurotransmitter systems are involved in pain modulation, it is possible age-related differences in CPM are due to functional changes in these systems in a number of areas within the neuroaxis.
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This paper describes the psychometric properties of the PROMIS-pain interference (PROMIS-PI) bank. An initial candidate item pool (n=644) was developed and evaluated based on the review of existing instruments, interviews with patients, and consultation with pain experts. From this pool, a candidate item bank of 56 items was selected and responses to the items were collected from large community and clinical samples. ⋯ The scores discriminated among persons with different numbers of chronic conditions, disabling conditions, levels of self-reported health, and pain intensity (p<0.0001). The results indicated that the PROMIS-PI items constitute a psychometrically sound bank. Computerized adaptive testing and short forms are available.
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This study aimed to identify distinctive trajectories for pain/disability and posttraumatic stress disorder (PTSD) symptoms following whiplash injury and to examine the effect of injury compensation claim lodgement on the trajectories. In a prospective study, 155 individuals with whiplash were assessed at <1month, 3, 6 and 12months post injury. Outcomes at each time point were Neck Disability Index (NDI) and the Posttraumatic Stress Diagnostic Scale (PDS). ⋯ Following whiplash injury, there are distinct pathways of recovery for pain/ disability and PTSD symptoms. Management of whiplash should consider the detrimental association of compensation claim with psychological recovery and recovery of those with mild to moderate pain/disability levels. However, claim lodgement has no significant association with a more severe pain and disability trajectory.