Articles: hyperalgesia.
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Cold-freeze injury at -4 degrees C to the rat sciatic nerve produces mechanical allodynia and thermal hyperalgesia [M. A. Kleive, P. ⋯ Injury to the rat sciatic nerve induced a significant increase in withdrawal frequency and a significant decrease in withdrawal latency (ANOVA, p<0.05). SYM-2081 and fentanyl significantly reduced these responses (p<0.05). These results suggest that kainate and opioid receptors are involved in the mechanical allodynia and thermal hyperalgesia that develop following cold injury to the sciatic nerve.
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Randomized Controlled Trial Clinical Trial
Low-dose lidocaine reduces secondary hyperalgesia by a central mode of action.
Sodium channel blockers are approved for intravenous administration in the treatment of neuropathic pain states. Preclinical studies have suggested antihyperalgesic effects on the peripheral as well as the central nervous system. The objective of this study was to determine mechanisms of action of low-dose lidocaine in experimental induced, secondary hyperalgesia. ⋯ In contrast, capsaicin-induced flare was significantly decreased after both treatments. We conclude that systemic lidocaine reduces pin-prick hyperalgesia by a central mode of action, which could involve blockade of terminal branches of nociceptors. A possible role for tetrodotoxin resistant sodium channels in the antihyperalgesic effect of low-dose lidocaine is discussed.
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Neuropathic pain is often resistant to opioids, so other medication classes, such as tricyclic antidepressants, anticonvulsants, and local anesthetics, are often used. Central sensitization, or pain 'wind-up', may perpetuate chronic neuropathic pain even when ongoing peripheral sensory input is absent. Wind-up is thought to cause allodynia, hyperalgesia, and hyperpathia. ⋯ No significant side effects were reported. Ketamine Gel may provide clinicians with a new option in the battle against chronic neuropathic pain. Until further information is available and larger trials can be conducted, we can only recommend this type of therapy for refractory cases in which all primary and secondary options have been exhausted.
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Reg Anesth Pain Med · Mar 2000
Comparative StudyLack of secondary hyperalgesia and central sensitization in an acute sheep model.
We aimed to determine the following in an experimental acute pain model in sheep: (1) whether multimodal analgesia with intravenous fentanyl and ketorolac was more effective than fentanyl alone; (2) whether secondary hyperalgesia (central sensitization) occurred in adjacent (foreleg) dermatomes after thoracic surgery; (3) whether ketorolac used preemptively influenced the development of secondary hyperalgesia after surgery. ⋯ The results obtained in this acute pain model found no significant evidence of a fentanyl-ketorolac interaction, of central sensitization as shown by secondary hyperalgesia, or of a preemptive analgesic effect.
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Neurological research · Mar 2000
Long-term intrathecal administration of glycine prevents mechanical hyperalgesia in a rat model of neuropathic pain.
Neuropathic pain has been postulated to be mediated, in part, by amino acid neurotransmitters including glycine. The current study examined the effects of continuous intrathecal glycine administration (0.1 mumol 0.5 microliter-1 h-1) on the development of mechanical hyperalgesia and other features of neuropathic pain evoked by unilateral loose ligation of the sciatic nerve in the rat. Each hind paw was tested for withdrawal threshold to mechanical stimuli prior to, and after ligation at intervals of 3, 6, 9, 12 and 16 days. ⋯ Glycine increased the normal mechano-nociceptive responses and prevented the development of mechano-nociceptive hyperalgesia. Spontaneous nociceptive behavior and hind paw dystrophic features, seen in the saline treated rats, were significantly diminished. Our results suggest that spinal cord inhibitory glycinergic activity is important for normal mechano-receptive responsitivity and development of mechano-nociceptive hyperalgesia in this model.