Pain
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The glial cytokine, interleukin-1beta (IL-1beta), potentiates the excitability of nociceptive trigeminal ganglion (TRG) neurons via membrane depolarization following peripheral inflammation. Perforated patch-clamp technique was used this study to show that the mechanism underlying the excitability of small-diameter TRG neurons following inflammation is due to IL-1beta. Inflammation was induced by injection of complete Freund's adjuvant (CFA) into the whisker pad. ⋯ IL-1beta inhibited I(A) to a significantly greater extent than I(K). These results suggest that the inhibitory effect of I(A) and I(K) currents by IL-1beta in small-diameter TRG neurons potentiates neuronal excitability thereby contributing to trigeminal inflammatory hyperalgesia. These findings provide evidence for the development of voltage-gated K(+) channel openers and IL-1beta antagonists as therapeutic agents for the treatment of trigeminal inflammatory hyperalgesia.
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Multicenter Study
Post-trauma ratings of pre-collision pain and psychological distress predict poor outcome following acute whiplash trauma: a 12-month follow-up study.
Patients with acute whiplash trauma were followed to examine if post-trauma ratings of pre-collision pain and psychological distress were associated with reduced work capability and neck pain at 12 months follow-up. The study included 740 consecutive patients (474 females, 266 males) referred from emergency departments or primary care after car accidents in four counties in Denmark. After the collision patients received a questionnaire on psychological distress, unspecified pain and socio-demographics and 12 months later a follow-up on work capability and neck pain was performed. ⋯ In conclusion unspecified as opposed to specified pain (neck pain) before the collision is associated with poor recovery and high accumulation of pre-collision psychological distress is associated with considerable neck pain at follow-up. However, no conclusions on causality can be drawn. Personal characteristics before the collision are important for recovery and attention to pre-collision characteristics may contribute to the prevention of poor recovery after acute whiplash trauma.
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Randomized Controlled Trial
Learning potentiates neurophysiological and behavioral placebo analgesic responses.
Expectation and conditioning are supposed to be the two main psychological mechanisms for inducing a placebo response. Here, we further investigate the effects of both expectation, which was induced by verbal suggestion alone, and conditioning at the level of N1 and N2-P2 components of CO2 laser-evoked potentials (LEPs) and subjective pain reports. Forty-four healthy volunteers were pseudorandomly assigned to one of three experimental groups: Group 1 was tested with verbal suggestion alone, Group 2 was tested with a conditioning procedure, whereby the intensity of painful stimulation was reduced surreptitiously, so as to make the volunteers believe that the treatment was effective, Group 3 was a control group that allowed us to rule out phenomena of sensitization and/or habituation. ⋯ Conversely, the N2-P2 amplitude changes that were induced by the conditioning procedure were associated with the subjective perception of pain reduction. Compared to natural history, conditioning produced more robust reductions of LEP amplitudes than verbal suggestions alone. Overall, these findings indicate that prior positive experience plays a key role in maximizing both behavioral and neurophysiological placebo responses, emphasizing that the placebo effect is a learning phenomenon which affects the early central nociceptive processing.
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Randomized Controlled Trial
Escitalopram in painful polyneuropathy: a randomized, placebo-controlled, cross-over trial.
Serotonin (5-HT) is involved in pain modulation via descending pathways in the central nervous system. The aim of this study was to test if escitalopram, a selective serotonin reuptake inhibitor (SSRI), would relieve pain in polyneuropathy. The study design was a randomized, double-blind, placebo-controlled cross-over trial. ⋯ Five patients (10.4%) discontinued the study because of adverse effects during escitalopram. This study found a pain-relieving effect of escitalopram in patients with painful polyneuropathy, but a clinically relevant effect was obtained in only few patients. Currently, the drug cannot be recommended as a standard treatment in neuropathic pain.
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Controlled Clinical Trial
Oral opioid use alters DNIC but not cold pain perception in patients with chronic pain - new perspective of opioid-induced hyperalgesia.
Opioids can elicit unexpected changes in pain sensitivity, known as opioid-induced hyperalgesia (OIH). The aim of this study was to explore whether OIH exists in patients with chronic pain treated with oral opioids (OP) versus non-opioid (NOP) analgesics. The sensitivity to cold pain and the magnitude of diffuse noxious inhibitory control (DNIC) were evaluated in 73 OP and 37 NOP treated patients. ⋯ A regression analysis showed that opioid dosage and treatment duration had a significant negative effect on the magnitude of DNIC in OP treated men (beta=-2.175, p=0.036 and beta=-2.061, p=0.047, respectively). In conclusion, oral opioids usage for the treatment of chronic pain does not result in abnormal sensitivity to cold pain, but seems to alter pain modulation. The use of 'advanced' psychophysics tests such as evaluation of DNIC can help understanding the phenomenon of OIH.