Articles: hyperalgesia.
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In the present study we determined the role of spinal 5-hydroxytriptamine (5-HT) and 5-HT(4/6/7) receptors in the long-term secondary mechanical allodynia and hyperalgesia induced by formalin in the rat. Formalin produced acute nociceptive behaviors (flinching and licking/lifting) followed by long-term secondary mechanical allodynia and hyperalgesia in both paws. In addition, formalin increased the tissue content of 5-HT in the ipsilateral, but not contralateral, dorsal part of the spinal cord compared to control animals. ⋯ In addition, these antagonists prevented the pro-nociceptive effect of ML-10302, EMD-386088 and LP-12, respectively. The i.t. post-treatment (6 days after formalin injection) with GR-125487, SB-258585 and SB-269970 reversed formalin-induced secondary allodynia and hyperalgesia in both paws. These results suggest that spinal 5-HT, released from the serotonergic projections in response to formalin injection, activates pre- or post-synaptic 5-HT(4/6/7) receptors at the dorsal root ganglion/spinal cord promoting the development and maintenance of secondary allodynia and hyperalgesia.
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Randomized Controlled Trial Clinical Trial
Interaction of fentanyl and buprenorphine in an experimental model of pain and central sensitization in human volunteers.
: There is controversy about combining opioids with different receptor affinities. We assessed the analgesic and antihyperalgesic effects of the μ-agonist fentanyl and the partial μ-agonist/κ-antagonist buprenorphine in a human pain model, when given alone or in combination. ⋯ : For the doses administered in this study, buprenorphine and fentanyl showed an additive interaction.
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Neuropathic pain refers to pain that arises as a direct consequence of a lesion or disease affecting the somatosensory nervous system.(1) Many cases of neuropathic pain run a chronic course, and treatment may be difficult because commonly used analgesics, including NSAIDs and to some extent opioids, are often ineffective. In addition, the use of other pharmacological treatments can be limited by unwanted effects. ⋯ This month and next month we review the drug treatment of neuropathic pain. In this first part we discuss neuropathic pain and the use of antidepressants.
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Review
Cold hyperalgesia as a prognostic factor in whiplash associated disorders: a systematic review.
To review and critically evaluate the existing literature for the prognostic value of cold hyperalgesia in Whiplash Associated Disorders (WAD). ⋯ There is moderate evidence supporting cold hyperalgesia as a prognostic factor for long-term pain and disability outcome in WAD. Further validation of the strength of this relationship and the influence of covariates are required. The mechanism for this relationship is unknown.
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The preprotachykinin A gene (ppt-A) codes for Substance P (SP), supports nociceptive sensitization, and modulates inflammatory responses after incision. Repeated opioid use produces paradoxical pain sensitization-termed opioid-induced hyperalgesia (OIH) -which can exacerbate pain after incision. Here the contribution of SP to peri-incisional nociceptive sensitization and nociceptive mediator production after opioid treatment was examined utilizing ppt-A knockout (-/-) mice and the neurokinin (NK1) receptor antagonist LY303870. Less mechanical allodynia was observed in ppt-A(-/-) mice compared to wild types (wt) after morphine treatment both before and after incision. Moreover, LY303870 administered with morphine reduced incisional hyperalgesia in wt mice. Incision after saline or escalating morphine treatment upregulated skin IL-1β, IL-6, G-CSF and MIP-1α levels in ppt-A(-/-) and wt mice similarly. However, chronic morphine treatment greatly exacerbated increases in skin nerve growth factor levels after incision, an effect entirely dependent upon intact SP signaling. Additionally, SP dependent upregulation of prodynorphin, NMDA1 and NK1 receptor expression in spinal cord was seen after morphine treatment and incision. A similar pattern was seen for 5-HT3 receptor expression in tissue from dorsal root ganglia. Therefore, SP may work at both central and peripheral sites to enhance nociceptive sensitization after morphine treatment and incision. ⋯ These studies show that SP signaling modulates enhanced nerve growth factor production and changes in neuronal gene expression seen after incision in mice previously exposed to morphine.