Pain
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Chronic musculoskeletal conditions are increasingly conceived as involving altered central nervous system processing, and impaired nociceptive flexor reflex (NFR) appears to reflect altered central nervous system processing. The primary objective was to synthesize the evidence for impaired NFR in these conditions. The secondary objective was to evaluate the NFR stimuli parameters employed by reviewed studies. ⋯ The results indicate that there is evidence of central hyperexcitability in people with chronic musculoskeletal pain. Our review also suggests that shorter inter-pulse duration tends to yield smaller variability in NFR threshold. However, further research investigating optimal stimulation parameters is still warranted.
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Review
Can pain be managed through the Internet? A systematic review of randomized controlled trials.
Given the increasing penetration and health care related use of the Internet, we examined the evidence on the impact of Internet-based interventions on pain. A search of Medline, CINAHL, PsycINFO, and the Cochrane Library was conducted for literature published from 1990 to 2010 describing randomized controlled trials that assessed the effects of Internet-based interventions on patients with pain of any kind. Of 6724 citations, 17 articles were included. ⋯ There was limited (n=2 from same research group) but promising evidence that Internet-based peer support programs can lead to improvements in pain intensity, activity limitation, health distress and self-efficacy; limited (n=4 from same research group) but promising evidence that social networking programs can reduce pain in children and adolescents; and insufficient evidence on Internet-based clinical support interventions. Internet-based interventions seem promising for people in pain, but it is still unknown what types of patients benefit most. More well-designed studies with diverse patient groups, active control conditions, and a better description of withdrawals are needed to strengthen the evidence concerning the impact of Internet-based interventions on people in pain.
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Pain after brachial plexus avulsion (BPA) is generally characterized by 2 main different components: paroxysmal (electrical shooting-like) pain, and continuous (burning) pain. Dorsal root entry zone (DREZ) lesioning, namely, the microsurgical DREZotomy (MDT) used in our practice, has proved to be a worthwhile neurosurgical treatment for this indication. However, according to previous studies, the method does not seem to demonstrate as good effectiveness in patients in whom the continuous background of pain was predominant as in patients with the paroxysmal component predominating. ⋯ Kaplan-Meier prediction of lasting global pain control at 120 months of follow-up was calculated at 41.1%. Comparison of the 2 corresponding Kaplan-Meier curves at long term, namely, pain control in 76.2% for the paroxysmal component and in 43.1% for the continuous component, showed a statistically significant difference (P=.038). Hypotheses for this relative differential effect are discussed.
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Interleukin-17 (IL-17) and tumour necrosis factor-α (TNF) are critical in the pathogenesis of arthritis but their relationship during inflammatory pain has received limited attention. We aimed to establish whether IL-17 can induce hyperalgesia in acute conditions, and investigated the role of TNF in mediating the pain response. Hyperalgesia was elicited in C57BL/6 mice by injection of recombinant IL-17, TNF or vehicle into the plantar tissue. ⋯ By means of an air pouch model of cell migration, it was established that IL-17-induced neutrophil infiltration was dependent of TNF/TNFR1 as this interaction was required for the induction of the chemokine keratinocyte chemoattractant. These findings suggest that IL-17 causes acute hyperalgesia indirectly by inducing TNF from resident cells. The subsequent production of keratinocyte chemoattractant then triggers neutrophil chemotaxis to the plantar tissue, releasing algesic mediators locally to sensitise the nerve.
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The transfer of nociceptive information at the level of dorsal horn is subject to extensive processing by both local segmental and supraspinal mechanisms, including descending dopaminergic controls, originating from the hypothalamic A11 nucleus. The inhibitory role of dopamine on evoked pain via activation of D2-like receptors at the level of the dorsal horn is well established. Here, by use of behavioral, electrophysiological, and anatomical techniques, we examined within the trigeminal sensory complex, first, whether descending dopaminergic controls also modulate pain behavior after an inflammatory insult, and second, under which physiological conditions these descending dopaminergic controls are actually recruited. ⋯ Altogether, our results are consistent with a tonic inhibition of the trigeminal nociceptive input by descending dopaminergic controls via activation of D2-like receptors at the level of superficial medullary dorsal horn. Such dopamine-dependent tonic inhibition of nociceptive information can be dynamically modulated by pain. This suggests that dysregulation of descending dopaminergic controls should translate in patients into diffuse, cephalic, and extracephalic pain symptoms--spontaneous pain, decreased pain thresholds, deficient DNIC, or some combination of these.