Articles: hyperalgesia.
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This study used streptozotocin (STZ; 50 mg/kg i.p.) diabetic rats and monitored weekly thermal and mechanical nociceptive thresholds for 8 weeks diabetes. Rats developed mechanical hyperalgesia as soon as 2 weeks after STZ injection. Thermal nociceptive threshold was not altered up to 8 weeks after STZ injection. ⋯ An increased release of glutamate and activation of the NMDA receptor, would maintain the hyperalgesic state. Reduced activity of both opioidergic and GABA(B)ergic inhibitory systems, might exacerbate the increased excitation thus contributing to the ongoing pain. It is suggested that NMDA receptor antagonists may constitute an alternative therapy for diabetic neuropathic pain.
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To investigate the role of Group I mGluRs in allodynia and hyperalgesia, we examined the behavioural responses of rats to noxious and non-noxious mechanical and thermal stimuli following intrathecal (i.t.) treatment (25 nmol) with the selective mGluR1/5 agonist, (RS)-dihydroxyphenylglycine ((RS)-DHPG). (RS)-DHPG administration produced a persistent decrease in response latency on a 48 degrees C hotplate, a reduction in the 50% response threshold to von Frey hairs, and an increase in responses to a tail pinch. These data suggest that activation of spinal mGluR1/5 receptors plays a role in the development of persistent allodynia and hyperalgesia associated with tissue or nerve injury.
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The paradoxical combination of sensory loss within the area where pain is felt together with pain evoked by non-noxious stimuli (allodynia) is a characteristic feature of neuropathic pain. This study examined the relationship between (mechanical and thermal) pain thresholds and dynamic and static hyperalgesia in 15 patients with traumatic nerve injury and brush-evoked pain. Sensory tests were carried out both in the allodynic skin area and in the unaffected contralateral mirror image skin. ⋯ There was no relationship between dynamic and static evoked hyperalgesia. These findings suggest a differential processing of repetitive thermal and mechanical stimuli in the central nervous system. Both dynamic and static mechanical hyperalgesia are maintained by activity in heat-sensitive nociceptors, but they are probably mediated by distinct mechanisms.
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Spinal neurons processing information from the ureter have been characterized in rats 1-4 days after the implantation of an experimental ureteric stone and compared with those of normal rats. The effects of a conditioning noxious stimulation of the ureter in the presence of the hyperalgesia evoked by the calculosis also were examined. Extracellular recordings were performed at the T12-L1 segments of the spinal cord. ⋯ A noxious ureteric distention applied to neurons with ureter input evoked a complex mixture of increases and decreases in somatic receptive field size and/or somatic input properties markedly different from the generalized increases in excitability seen when such a stimulus was applied to normal animals. We conclude that the presence of a ureteric stone evokes excitability changes of spinal neurons (enhanced background activity, greater number of ureter-driven cells, decreased threshold of convergent somatic receptive fields), which likely account for the referred hyperalgesia seen in rats with calculosis. However, further noxious visceral input occurring in the presence of persistent hyperalgesia produces selective changes that cannot be explained by a generalized excitability increase and suggest that the mechanisms underlying maintenance of hyperalgesia include alteration of both central inhibitory and excitatory systems.
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Anesthesia and analgesia · Mar 1998
The effect of electroconvulsive treatment on thermal hyperalgesia and mechanical allodynia in a rat model of peripheral neuropathy.
We tested the ability of electroconvulsive treatment (ECT) to block thermal hyperalgesia and mechanical allodynia in rats with peripheral neuropathy. Repeated ECT (six times daily) significantly reduced thermal hyperalgesia 48 h after the end of the final treatment but had no significant effects on mechanical allodynia. Single ECT had no significant effect on thermal hyperalgesia or mechanical allodynia. Neither single nor repeated ECT had any significant effect on the withdrawal response of sham-operated paws and untreated rats to thermal and mechanical stimuli. The anti-thermal hyperalgesic effect of repeated ECT was reversed by the previous administration of nifedipine (L-type Ca2+ channel blocker). We conclude that, due to effects on the voltage dependent calcium channel, ECT modified one of the pain behaviors induced by nerve injury. ECT may be of use in the treatment of human neuropathic pain. ⋯ We showed that repeated electroconvulsive treatment reduced pain responses to heat stimulation after sciatic nerve injury in rats. This study implies a possible therapeutic effect of electroconvulsive treatment on neuropathic pain.