Pain
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It has been proposed that painful and non-painful referred sensations (RSs) are associated with reorganization of sensory pathways in patients with complete spinal cord injury (SCI). In order to investigate the referred sensation (RS) phenomenon and its correlation with neuropathic pain (NP) 48 patients with complete SCI, 24 with chronic NP and 24 without pain or paraesthesias were studied using clinical examination and neurophysiological tests. Patients reporting RSs were re-examined at 2 and 10weeks after the first examination. ⋯ None of the patients in the SCI group without NP presented RS. In conclusion, our results indicate that RS is relatively frequent in patients with complete SCI and NP. The common occurrence of RS in patients with NP and the location of the sensations in the same area as NP suggest that pain and RS share common pathophysiological mechanisms.
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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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Behavioral studies have suggested that placebo analgesia is partly mediated by the endogenous opioid system. Expanding on these results we have shown that the opioid-receptor-rich rostral anterior cingulate cortex (rACC) is activated in both placebo and opioid analgesia. However, there are also differences between the two treatments. ⋯ Furthermore, the rACC activity co-varied with the prefrontal regions in the placebo condition specifically. A similar correlation between rACC and vlPFC was reproduced in another dataset involving emotional placebo and correlated with the degree of the placebo effect. Our results thus support that placebo is different from specific treatment with a prefrontal top-down influence on rACC.
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Injection of hypertonic saline into back muscles or ligaments can induce acute low back pain (LBP). However, no study has systematically investigated pain characteristics from these structures. Further, induced muscle pain can change with stretching and contraction, which is problematic for studies into the effect of pain on sensorimotor control. ⋯ Surprisingly, some participants pointed to a location of pain that was 1-2 segments above or below the injected level. The results highlight that injection into the interspinous ligament elicits consistent pain that is not influenced by trunk movements. These findings support the implementation of this experimental ligament pain model in research.
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We tested whether it is possible to selectively block pain signals in the orofacial area by delivering the permanently charged lidocaine derivative QX-314 into nociceptors via TPRV1 channels. We examined the effects of co-applied QX-314 and capsaicin on nociceptive, proprioceptive, and motor function in the rat trigeminal system. QX-314 alone failed to block voltage-gated sodium channel currents (I(Na)) and action potentials (APs) in trigeminal ganglion (TG) neurons. ⋯ Co-application of QX-314 and capsaicin inhibited the jaw-opening reflex evoked by noxious electrical stimulation of the tooth pulp when applied to a sensory but not a motor nerve, and produced long-lasting analgesia in the orofacial area. These data show that selective block of pain signals can be achieved by co-application of QX-314 with TRPV1 agonists. This approach has potential utility in the trigeminal system for treating dental and facial pain.