Pain
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Comparative Study
Numbness in clinical and experimental pain--a cross-sectional study exploring the mechanisms of reduced tactile function.
Pain patients often report distinct numbness of the painful skin although no structural peripheral or central nerve lesion is obvious. In this cross-sectional study we assessed the reduction of tactile function and studied underlying mechanisms in patients with chronic pain and in healthy participants exposed to phasic and tonic experimental nociceptive stimulation. Mechanical detection (MDT) and pain thresholds (MPT) were assessed in the painful area and the non-painful contralateral side in 10 patients with unilateral musculoskeletal pain. ⋯ Irrespective of the mode of nociceptive stimulation (phasic vs. tonic) tactile hypaesthesia and hyperalgesia developed with a similar time course and disappeared within approximately 1 day. Hypaesthesia (numbness) often encountered in clinical pain can be reproduced by experimental nociceptive stimulation. The time course of effects suggests a mechanism involving central plasticity.
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Transient receptor potential vanilloid 1 (TRPV1) is highly expressed in primary afferent neurons. Tissue damage generates an array of chemical mediators that activate and sensitize afferent nerve fibers, and sensitization of afferent nerve fibers plays an important role in development of visceral pain. We investigated participation of TRPV1 in visceral pain associated with bladder inflammation induced in mice by systemic treatment with cyclophosphamide or intravesical instillation of acrolein. ⋯ Cystitis did not affect the threshold of response to thermal stimuli in WT or KO mice. These results suggest that TRPV1 is essential for cystitis-induced bladder mechanical hyperreactivity. Also, TRPV1 participates in development of visceral pain, as reflected by referred increased mechanosensitivity in peripheral tissues in the presence of visceral inflammation.
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Comparative Study
Estimation of pain intensity in emergency medicine: a validation study.
This study was designed to estimate the validity of an 11-point verbal numerical rating scale (VNRS) and a 100 Unit (U) plasticized visual analogue scale (VASp) using a 100mm paper visual analogue scale (VAS) as a gold standard, to recommend the best method of reporting the intensity of acute pain in an emergency department (ED). A convenience sample of 1176 patients with acute pain were recruited in the ED of a teaching hospital. Patients >18 years and able to use the different scales were included. ⋯ In conclusion, the VASp has a small bias, acceptable limits of agreement and an excellent intra-class correlation. It is probably a valid tool to estimate acute pain in the ED. However, the VNRS is less valid in that context because of its wide limits of agreement and variable bias (mainly in lower scores).
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Comparative Study
The spatial characteristics of the painful thermal grill illusion.
Interlaced cold and warm stimuli may induce a paradoxical burning sensation termed the "thermal grill illusion". Studies on the grill illusion have yielded contradictory results regarding its quality and intensity, which in turn led to controversies concerning the underlying mechanism. Some controversies may result from testing the illusion with absolute temperatures thereby disregarding inter-subjects' variation in temperature sensitivity. ⋯ Gender did not affect the PGI. In conclusion, innocuous cold and warm stimuli can spatially summate, both within and between dermatomes and evoke a PGI. Possibly, non-nociceptive channels integrate onto 2nd or 3rd order nociceptive neurons which in turn induce a unique painful burning resulting from the blend of cold and warm sensations.
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It is increasingly recognized that pain-induced plasticity may not only provoke sensory gain (hyperalgesia), but also sensory decline, i.e. hypoesthesia and hypoalgesia. We investigated perceptual changes by conditioning electrical stimulation of peptidergic C-nociceptors differing in stimulation frequencies and duty cycles at the left forearm. Four noxious electrical stimulation paradigms (Stim1: 0.5 Hz, continuously; Stim2: 20 Hz, continuously; Stim3: 1s 20 Hz train, 1s break; Stim4: 1s 20 Hz train, 2s break) were applied. ⋯ In summary, we describe here that depending on the applied frequencies and duty cycles, either sensory gain (i.e. hyperalgesia) or sensory decline (i.e. hypoesthesia and hypoalgesia) can be induced. Sensory decline was found to be centrally mediated. Underlying mechanisms may include differential recruitment of inhibitory and facilitating gain control systems leading to homo- and heterosynaptic inhibition or facilitation at the level of the spinal cord or interference of noxious input with tactile processing in the cortex.