Articles: hyperalgesia.
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Tissue injury results in the release of inflammatory mediators, including a cascade of nociceptive substances, which contribute to development of hyperalgesia. In addition, during this process endogenous analgesic substances are also peripherally released with the aim of controlling the hyperalgesia. Thus, the present study aimed to investigate whether inflammatory mediators TNF-α, IL-1β, CXCL1, norepinephrine (NE) and prostaglandin E2 (PGE2) may be involved in the deflagration of peripheral endogenous modulation of inflammatory pain by activation of the opioid system. ⋯ In contrast, when the enzyme N-aminopeptidase involved in the degradation of endogenous opioid peptides was inhibited by bestatin, the hyperalgesia was significantly reduced. In addition, the western blotting assay indicated that the expression of the opioid δ receptor was increased after intraplantar injection of carrageenan. The data obtained in this work corroborate the hypothesis that TNF-α, CXCL-1 and IL-β cause, in addition to hyperalgesia, the release of endogenous substances such as opioid peptides, which in turn exert endogenous control over peripheral inflammatory pain.
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The mechanisms underlying pain modulation by hypnosis and the contribution of hypnotic induction to the efficacy of suggestions being still under debate, our study aimed, (1) to assess the effects of identical hypoalgesia suggestions given with and without hypnotic induction, (2) to compare hypnotic hypoalgesia to distraction hypoalgesia and (3) to evaluate whether hypnotic suggestions of increased and decreased pain share common psychophysiological mechanisms. To this end, pain ratings, nociceptive flexion reflex amplitude, autonomic responses and electroencephalographic activity were measured in response to noxious electrical stimulation of the sural nerve in 20 healthy participants, who were subjected to four conditions: suggestions of hypoalgesia delivered with and without hypnosis induction (i.e. hypnotic-hypoalgesia and suggested-hypoalgesia), distraction by a mental calculation task and hypnotic suggestions of hyperalgesia. As a result, pain ratings decreased in distraction, suggested-hypoalgesia and hypnotic-hypoalgesia, while it increased in hypnotic-hyperalgesia. ⋯ The absence of a significant difference between the hypnotic hypoalgesia and hyperalgesia conditions suggests that brain processes as evidenced by evoked potentials are not invariably related to pain modulation. Time-frequency analysis of electroencephalographic activity showed a significant differentiation between distraction and hypnotic hypoalgesia in the theta domain. These results highlight the diversity of neurophysiological processes underlying pain modulation through different psychological interventions.
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Spinal cord stimulation (SCS) is a recommended treatment for chronic neuropathic pain. Persistent nonoperative low back pain of neuropathic origin has profound negative impacts on patient's lives. This prospective, open label, research study aimed to explore the use of SCS in patients with associated features of central sensitisation such as allodynia and hyperalgesia. ⋯ The 10 kHz SCS improved back and leg pain, QoL, pain-related disability and medication consumption in patients with nonoperative back pain of neuropathic origin. With further research incorporating a sham control arm, the efficacy of 10 kHz SCS in this patient cohort will become more established.
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Trigeminal neuropathic pain is the most debilitating pain disorder but current treatments including opiates are not effective. A common symptom of trigeminal neuropathic pain is cold allodynia/hyperalgesia or cold hypersensitivity in orofacial area, a region where exposure to cooling temperatures are inevitable in daily life. Mechanisms underlying trigeminal neuropathic pain manifested with cold hypersensitivity are not fully understood. ⋯ Here, we created infraorbital nerve chronic constrictive injury (ION-CCI) in rats, an animal model of trigeminal neuropathic pain to show that dysfunction of Kv4.3 voltage-gated K+ channels in nociceptive-like trigeminal ganglion (TG) neurons underlies the trigeminal neuropathic pain manifested with cold hypersensitivity in orofacial regions. Furthermore, we demonstrate that pharmacological potentiation of Kv4.3 channels can alleviate orofacial cold hypersensitivity in ION-CCI rats. Our results may have clinical implications in trigeminal neuropathic pain in human patients, and Kv4.3 channels may be an effective therapeutic target for this devastating pain disorder.