Pain
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Randomized Controlled Trial Clinical Trial
Deciphering the role of endogenous opioids in high-frequency TENS using low and high doses of naloxone.
Previous human studies have shown that the analgesic effect of high-frequency TENS could not be reversed by low doses of naloxone. The aim of the present study was to reinvestigate the possible contribution of opioid receptors to high-frequency TENS analgesia by using low (0.02 mg/kg) and high (0.14 mg/kg) doses of naloxone. Naloxone (high and low doses) and saline were administered intravenously to young healthy adults using a triple-blind randomized cross-over design. ⋯ However, when a high dose of naloxone was administered, TENS analgesia was completely blocked (p=.20). These results suggest that high-frequency TENS involves opioid receptors. An insufficient amount of opioid antagonist likely prevented previous human studies from discovering the importance of opioid receptors in producing high-frequency TENS analgesia.
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Evidence from clinic-based studies suggests that the fibromyalgia syndrome (FMS) is associated with impairment in cognitive function though the mechanism is unclear. The aim of this analysis was to determine whether there is a similar association between chronic widespread pain (CWP), a cardinal feature of FMS, and impaired cognition in a community setting. Men (n=3369, 40-79 years) were recruited from population registers in eight centres for participation in the European Male Ageing Study (EMAS). ⋯ There was no association between CWP and the ROCF-copy, ROCF-recall or CTRM scores. CWP is associated with slower psychomotor processing speed among community-dwelling European men. Prospective studies are required to confirm this observation and explore possible mechanisms for the association.
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Clinical Trial
Neuronal mechanisms during repetitive trigemino-nociceptive stimulation in migraine patients.
Habituation deficits in various sensory modalities have been observed in migraine patients in several experimental designs. The underlying neuronal mechanisms are, however, still unknown. Past studies have used electrophysiological measures and focussed on habituation behaviour during one single session. ⋯ These data suggest that several brain areas known to be involved in endogenous pain control show a completely opposite behaviour in migraine patients compared to healthy controls. These brain networks seem not to be disrupted per se in migraine patients but changed activity over time responding to repetitive nociceptive input. The alteration of pain inhibitory circuits may be the underlying mechanism responsible for the dys-functional neuronal filters of sensory input.
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The aim of this study was to investigate how exercise influenced endogenous pain modulation in healthy controls, shoulder myalgia patients and fibromyalgia (FM) patients. Twenty-one healthy subjects, 20 shoulder myalgia patients and 20 FM patients, all females, participated. They performed standardized static contractions, that is, outward shoulder rotation (m. infraspinatus) and knee extension (m. quadriceps). ⋯ During contraction of m. quadriceps PPTs increased compared to baseline at the end of contraction in healthy controls (all sites: p<0.001) and myalgia patients (all sites: p<0.02), but not in FM patients. In conclusion, we found a normal activation of endogenous pain regulatory mechanisms in myalgia patients during contraction of the non-afflicted m. quadriceps, but a lack of pain inhibition during contraction of the painful m. infraspinatus. FM patients failed to activate their pain inhibitory mechanisms during all contractions.
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NMDA receptors have an important role in pain facilitation in rostral ventromedial medulla (RVM) and the NR1 subunit is essential for its function. Studies suggest that the NMDA receptors in RVM are critical to modulate both cutaneous and muscle hypersensitivity induced by repeated intramuscular acid injections. We propose that increased expression of the NR1 subunit in the RVM is critical for the full development of hypersensitivity. ⋯ We also downregulated the expression of NR1 in the RVM and measured the hyperalgesia produced by repeated-acid injections. Increasing the expression of NR1 in the RVM reduces cutaneous and muscle withdrawal threshold, and decreasing the expression of NR1 in the RVM increases the muscle withdrawal threshold and prevents the development of hyperalgesia in an animal model of muscle pain. These results suggest that the NR1 subunits in the RVM are critical for modulating NMDA receptor function, which in turn sets the 'tone' of the nervous system's response to noxious stimuli and tissue injury.