Articles: hyperalgesia.
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Anesthesia and analgesia · Dec 1999
Randomized Controlled Trial Clinical TrialThe effects of intradermal fentanyl and ketamine on capsaicin-induced secondary hyperalgesia and flare reaction.
In this study, we evaluated the effects of intradermal fentanyl and ketamine on capsaicin-induced hyperalgesia and axon-reflex flare. In addition, we obtained dose-response curves for possible local anesthetic effects. Saline (200 microL) and either fentanyl (1 microg or 10 microg in 200 microL) or ketamine (100 microg or 1000 microg in 200 microL) were injected simultaneously into the central volar forearm of 12 healthy volunteers. Nine minutes later, capsaicin (10 microg in 20 microL) was injected intracutaneously exactly between the two injection sites. Areas of touch-evoked allodynia and pinprick hyperalgesia, as well as intensity of pinprick hyperalgesia at the injection sites and axon-reflex flare, were evaluated. Fentanyl did not affect the area or intensity of secondary hyperalgesia. Only the larger concentration of fentanyl locally diminished axon-reflex flare without affecting mechanical detection thresholds. Inhibitory effects of ketamine on intensity of secondary hyperalgesia and axon reflex flare were observed only in the larger concentration. However, this concentration also clearly elevated mechanical detection thresholds. No inhibitory effects of ketamine in the smaller concentrations were observed. We conclude that fentanyl inhibits neuropeptide release on peripheral application without modulating secondary hyperalgesia. Ketamine failed to inhibit both secondary hyperalgesia and axon reflex flare as long as nonlocal anesthetic concentrations were applied. ⋯ We investigated the peripheral effects of fentanyl and ketamine on capsaicin-induced hyperalgesia and axon-reflex flare. In large concentrations, the opioid diminished axon-reflex flare without effects on secondary hyperalgesia. We found no evidence for the involvement of endogenous glutamate in secondary hyperalgesia or axon reflex flare.
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Tissue injury induces enhanced pain sensation to light touch and punctate stimuli in adjacent, uninjured skin (secondary hyperalgesia). Whereas hyperalgesia to light touch (allodynia) is mediated by A-fibre low-threshold mechanoreceptors, hyperalgesia to punctate stimuli may be mediated by A- or C-fibre nociceptors. To disclose the relative contributions of A- and C-fibres to the hyperalgesia to punctate stimuli, the superficial radial nerve was blocked by pressure at the wrist in nine healthy subjects. ⋯ In conclusion, the pricking pain to punctate stimuli is predominantly mediated by A-fibre nociceptors. In secondary hyperalgesia, this pathway is heterosynaptically facilitated by conditioning C-fibre input. Thus, secondary hyperalgesia to punctate stimuli is induced by nociceptive C-fibre discharge but mediated by nociceptive A-fibres.
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Chronic compression of the dorsal root ganglion (CCD) was produced in adult rats by implanting a stainless steel rod unilaterally into the intervertebral foramen, one rod at L(4) and another at L(5). Two additional groups of rats received either a sham surgery or an acute injury consisting of a transient compression of the ganglion. Withdrawal of the hindpaw was used as evidence of a nocifensive response to mechanical and thermal stimulation of the plantar surface. ⋯ Ectopic spontaneous discharges generated within the chronically compressed ganglion and, occurring in the absence of blood-borne chemicals and without an intact sympathetic nervous system, were recorded from neurons with intact, conducting, myelinated or unmyelinated peripheral nerve fibers. The incidence of spontaneously active myelinated fibers was 8.61% for CCD rats versus 0.96% for previously nonsurgical rats. We hypothesize that a chronic compression of the dorsal root ganglion after certain injuries or diseases of the spine may produce, in neurons with intact axons, abnormal ectopic discharges that originate from the ganglion and potentially contribute to low back pain, sciatica, hyperalgesia, and tactile allodynia.
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Anesthesia and analgesia · Dec 1999
Comparative StudyHyperalgesia caused by nerve transection: long-lasting block prevents early hyperalgesia in the receptive field of the surviving nerve.
The aim of our study was to test the hypothesis that a long-lasting N-butyl tetracaine nerve block (>2 wk) would be much more effective in the prevention of hyperalgesia caused by nerve transection than the short-lasting lidocaine block. The study was performed with the use of the saphenous nerve section model in rats. The saphenous nerve was exposed and injected with saline, lidocaine (37 mM), or N-butyl tetracaine (37 mM). Ten minutes later, the nerve was transected in some of the rats. The development of mechanical hyperalgesia (pressure threshold) of the hindpaw was assessed during a 5-wk period. In rats with saphenous nerve transection without nerve block (saline injection), 3 h after the transection, the pressure threshold decreased by approximately 30% (from 175+/-11 g to 122+/-23 g, P < 0.0001); the threshold increased somewhat the next day, then it remained stable for 2 wk, with a slow process of recovery afterward. N-butyl tetracaine block without nerve transection caused a slow-developing decrease in the pressure threshold with the first statistically significant change at the sixth day. The comparison of the preventive effects of lidocaine and N-butyl tetracaine blocks on early hyperalgesia caused by nerve transection demonstrated that both lidocaine and N-butyl tetracaine prevented hyperalgesia 3 h after the transection. However, the protective effect of lidocaine disappeared the next day. In contrast, N-butyl tetracaine prevented early hyperalgesia for almost a week. The slow-developing late hyperalgesia caused by long-lasting nerve block makes it impossible to study the protective effect of such a block on late hyperalgesia caused by axotomy. As far as early hyperalgesia is concerned, the preventive effect of the N-butyl tetracaine was much longer than that of lidocaine and continued for approximately 1 wk. ⋯ A long-lasting nerve block can prevent early hyperalgesia caused by nerve transection.
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Painful peripheral neuropathies involve both axonal damage and an inflammation of the nerve. The role of the latter by itself was investigated by producing an experimental neuritis in the rat. The sciatic nerves were exposed at mid-thigh level and wrapped loosely in hemostatic oxidized cellulose (Oxycel) that on one side was saturated with an inflammatory stimulus, carrageenan (CARRA) or complete Freund's adjuvant (CFA), and on the other side saturated with saline. ⋯ The neuropathic pain is specific to inflammation of the nerve because it was absent in animals with the experimental myositis and in those receiving sham-treatment. These results suggest that an acute episode of neuritis-evoked neuropathic pain may contribute to the genesis of chronically painful peripheral neuropathies, and that a chronic (or chronically recurrent) focal neuritis might produce neuropathic pain in the absence of significant (or clinically detectable) structural damage to the nerve. The model that we describe is likely to be useful in the study of the neuroimmune factors that contribute to painful peripheral neuropathies.