Articles: hyperalgesia.
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Injured sensory axons trapped in a neuroma or freely regenerating in the distal nerve stump, frequently display ectopic mechanosensitivity, spontaneous impulse discharge or both. This abnormal neural activity is thought to contribute to spontaneous and movement-evoked neuropathic paraesthesias, dysaesthesias and pain, as well as to allodynia and hyperalgesia. ⋯ This suggests that mechanosensitivity and spontaneous firing are aspects of a single underlying pathophysiological process. Copyright 1998 European Federation of Chapters of the International Association for the Study of Pain.
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Experimental neurology · Jan 1998
A neuronal correlate of secondary hyperalgesia in the rat spinal dorsal horn is submodality selective and facilitated by supraspinal influence.
Tissue injury produces hyperalgesia not only in the injured area (primary hyperalgesia) but also outside of it (secondary hyperalgesia). In the present investigation, the submodality selectivity and the contribution of supraspinal influence to a neural correlate of the secondary hyperalgesia induced by neurogenic inflammation was studied in the presumed pain relay neurons of the rat spinal dorsal horn. Mechanically and thermally evoked responses to wide-dynamic range (WDR) neurons of the spinal dorsal horn were recorded under sodium pentobarbital anesthesia in rats. ⋯ The selective mechanical hyperexcitability in spinal WDR neurons, without a change in their spontaneous activity, can be explained by a heterosynaptic facilitatory action on presynaptic terminals mediating mechanical signals to these nociceptive spinal neurons. These findings indicate that brain stem-spinal pathways, involving the RVM, do not only suppress nociception but under some pathophysiological conditions concurrent facilitatory influence may predominate and lead to enhancement of mechanical hyperexcitability. The descending facilitatory feed-back loop to nociceptive spinal neurons may help to protect the wounded tissue and thus promote healing.
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The authors sought to characterize the pharmacologic characteristic and site of action of gabapentin (Neurontin) in a model of thermal hyperalgesia induced by intrathecal substance P administration. ⋯ The structure-activity relationship and the stereospecificity noted after intrathecal delivery suggest that gabapentin and S(+)-3-isobutyl-gamma aminobutyric acid act at a common spinal locus to modulate selectively a facilitated state of nociceptive processing.
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Recent evidence suggests that the duration of the nociceptive block may be an important factor in determining the effect of the block on injury-induced hyperalgesia after block resolution. The authors examined whether a tonicaine nerve block lasting for 12 to 16 h could prevent late inflammatory hyperalgesia. ⋯ A prolonged nerve block (12-16 h) can prevent the development of long-lasting (3-5 days) inflammatory hyperalgesia. Prevention of late hyperalgesia can be provided not only by the preinjury block but also by the postinjury block administered when hyperalgesia is already well established.
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Neurotropin is commonly used in Japan for the treatment of chronic pain. Using a rat model, we evaluated the effect of neurotropin on a unilateral peripheral mononeuropathy produced by placing loose ligatures around the sciatic nerve. ⋯ No significant reduction in mechanical allodynia, however, was noted under the tested condition. A possibility of differential drug sensitivity for thermal hyperalgesia and mechanical allodynia was indicated in this model, although the reason still remain elusive.