Articles: hyperalgesia.
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Randomized Controlled Trial Clinical Trial
Postdelivery of alfentanil and ketamine has no effect on intradermal capsaicin-induced pain and hyperalgesia.
The predelivery of intravenous alfentanil (a mu opioid agonist) and ketamine (an -methyl d-aspartate antagonist) has recently been shown to decrease the secondary hyperalgesia induced by intradermal capsaicin. The focus of this study was to determine the effects of the postdelivery of intravenous alfentanil and ketamine on intradermal capsaicin-induced secondary hyperalgesia. ⋯ Consistent with animal studies on preemptive analgesia, this study demonstrates that alfentanil and ketamine have a differential effect when delivered before and after a painful stimulus. Because of the differential effect seen, future studies on the pharmacology of human experimental pain should evaluate both predrug and postdrug delivery.
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Randomized Controlled Trial Clinical Trial
Experimental incision-induced pain in human skin: effects of systemic lidocaine on flare formation and hyperalgesia.
In order to try to gain a better understanding of the mechanisms of post-operative pain, this study was designed to psychophysically determine physiological and pharmacological characteristics of experimental pain induced by a 4-mm-long incision through the skin, fascia and muscle in the volar forearm of humans. In experiment 1, the subjects (n=8) were administered lidocaine systemically (a bolus injection of 2mg/kg for a period of 5 min followed by an intravenous infusion of 2mg/kg/h for another 40 min), and then the incision was made. In experiment 2, cumulative doses of lidocaine (0.5-2mg/kg) were systemically injected in the subjects (n=8) 30 min after the incision had been made, when primary and secondary hyperalgesia had fully developed. ⋯ Pre-traumatic treatment with lidocaine would temporarily stabilize the sensitized nerves in the injured area, but the nerves would be sensitized after completion of the administration. Post-traumatic treatment with lidocaine reduced primary and secondary hyperalgesia that had fully developed. However, the finding that the suppressive effect of lidocaine on secondary hyperalgesia was temporary suggests that the development and maintenance of secondary hyperalgesia are caused by different mechanisms.
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The herpes zoster rash occurs when a dormant varicella zoster virus reactivates in dorsal root and cranial nerve ganglia. Pain that persists in the region where this rash occurred after the cutaneous lesions have healed is termed postherpetic neuralgia (PHN). A wide variety of therapies has been used with varying degrees of success to prevent the occurrence of PHN and to reduce pain with established PHN. ⋯ Several classes of drugs are effective in attenuating the pain and hyperalgesia caused by PHN, but no single drug leads to the complete relief of symptoms. Additional research is needed to improve treatment strategies and define the role of invasive pain management techniques in cases where PHN is associated with intractable pain.
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Neuropathic pain syndromes are characterized by spontaneous pain and by stimulus-evoked allodynia and hyperalgesia. Stimulus-induced pain, i.e. the capacity of external stimuli to alter sensory processing so as to generate a pain hypersensitivity that outlasts the initiating stimulus, is usually present only after intense activation of nociceptors. In abnormal pain states, however, such as after capsaicin injection or inflammation, a stimulus-induced incremental pain can be generated by repetitive light touch, termed progressive tactile hypersensitivity (PTH). ⋯ However, 10 weeks and after, the same repeated stimulation induced a progressive tactile hypersensitivity that persisted after discontinuation of the tactile stimulation. Following SNI, repeated stimulation of the hypersensitive skin territory, corresponding to the intact spared sural nerve, never induced PTH. Tactile stimulation of regenerating afferents but not spared non-injured afferents, can induce, therefore, PTH and such a stimulus-induced alteration in pain processing may contribute to clinical neuropathic pain.