Pain
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Randomized Controlled Trial
Effects of spatially targeted transcutaneous electrical nerve stimulation using an electrode array that measures skin resistance on pain and mobility in patients with osteoarthritis in the knee: a randomized controlled trial.
A novel device was developed that measured local electrical skin resistance and generated pulsed local electrical currents that were delivered across the skin around the knee for patients with osteoarthritis (termed eBrace TENS). Currents were delivered using an electrode array of 16 small circular electrode elements so that stimulation could be spatially targeted. The aim of this study was to investigate the effects of spatially targeted transcutaneous electrical nerve stimulation (TENS) to points of low skin resistance on pain relief and mobility in osteoarthritis of the knee (OAK). ⋯ Lowest-resistance TENS reduced pain intensity during walking relative to resting baseline compared with random TENS (95% confidence interval of the difference: -20.8mm, -1.26 mm). There were no statistically significant differences between groups in distance during the walk test, maximum voluntary contraction (MVC) or range-of-motion (ROM) measures or WOMAC scores. In conclusion, we provide evidence that use of a matrix electrode that spatially targets strong nonpainful TENS for 30 to 45 minutes at sites of low resistance can reduce pain intensity at rest and during walking.
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We performed a prospective study in 32 patients with Guillain-Barré syndrome (GBS) or its variants to correlate intraepidermal nerve fiber density (IENFD) at the distal leg and lumbar region with pain, autonomic dysfunction, and outcome. In the acute phase, IENFD was reduced in 60% and 61.9% of patients at the distal leg and lumbar region, respectively. In the acute phase, 43.7% of patients complained of neuropathic pain. ⋯ Double and triple staining confocal microscope studies showed diffuse damage of myelinated dermal nerves along with axonal degeneration, and mononuclear cell infiltration. Unmyelinated and myelinated skin nerves are diffusely affected in GBS and its variants, including the pure motor form. IENFD declines early, remains low over time, correlates with pain severity in the acute phase, and may predict long-term disability.
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Menthol is a natural compound of plant origin known to produce cool sensation via the activation of the TRPM8 channel. It is also frequently part of topical analgesic drugs available in a pharmacy, although its mechanism of action is still unknown. Compelling evidence indicates that voltage-gated Na(+) channels are critical for experiencing pain sensation. ⋯ In current clamp recordings, menthol inhibited firing at high-frequency stimulation with minimal effects on normal neuronal activity. We found that low concentrations of menthol cause analgesia in mice, relieving pain produced by a Na(+) channel-targeting toxin. We conclude that menthol is a state-selective blocker of Nav1.8, Nav1.9, and TTX-sensitive Na(+) channels, indicating a role for Na(+) channel blockade in the efficacy of menthol as topical analgesic compound.
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Comparative Study
Differential effects of experimental central sensitization on the time-course and magnitude of offset analgesia.
Pain perception is temporally altered during states of chronic pain and acute central sensitization; however, the mechanisms contributing to temporal processing of nociceptive information remain poorly understood. Offset analgesia is a phenomenon that reflects the presence of temporal contrast mechanisms for nociceptive information and can provide an end point to study temporal aspects of pain processing. In order to investigate whether offset analgesia is disrupted during sensitized states, 23 healthy volunteers provided real-time continuous visual analogue scale responses to noxious heat stimuli that evoke offset analgesia. ⋯ Increased latencies to maximal offset analgesia and prolonged aftersensations were observed only in the primary regions directly treated by capsaicin-heat or heat alone. However, contrary to the hypothesis that offset analgesia would be reduced following capsaicin-heat sensitization, the magnitude of offset analgesia remained remarkably intact after both capsaicin-heat and heat-only sensitization in zones of both primary and secondary mechanical allodynia. These data indicate that offset analgesia is a robust phenomenon and engages mechanisms that interact minimally with those supporting acute central sensitization.