Articles: hyperalgesia.
-
Various hypotheses have been proposed to account for the mechanical hyperalgesia and spontaneous pain seen in animal models of peripheral neuropathy. The purpose of the present study was to determine whether there exists a spinal neuronal correlate to these properties. An experimental neuropathy was induced in male Sprague-Dawley rats by placing a 2-mm PE-90 polyethylene cuff around the sciatic nerve. ⋯ There may be a redistribution of membrane-bound ion channels, predominantly sodium channels, which leads to ectopic activity and thus spontaneous discharge of dorsal horn neurons. With regard to mechanical stimulation-evoked synaptic input, the central terminals of myelinated afferents expand into regions of the spinal cord which normally receive their predominant input from unmyelinated nociceptive afferents. This may be coupled with a change in these myelinated afferents so that they now synthesize and release peptides, primarily substance P, from their central terminals with the result that the effects of their chemical mediators of synaptic transmission add to the effects of nociceptive inputs leading to exaggerated responses to painful stimuli, thus the basis of clinical hyperalgesia.
-
Human experimental pain models are important tools in pain research. The primary aims of pain research in normal man is 1) to provide insight in pain mechanisms, 2) to provide a rational basis for clinical trials of pain relieving interventions, and 3) to confirm the anti-nociceptive effects demonstrated in animal models. Most often clinical pain is due to tissue damage leading to acute inflammation and hyperalgesia, but only few human pain models have examined pain responses in injured tissues. ⋯ A contribution from sensitised CNS neurones is likely, and the sensitisation of nociceptors is confined to the injured area. The presence of hyperalgesia to heat in normal skin surrounding a burn (secondary hyperalgesia) has been demonstrated in several studies, but the pain threshold may be unaltered. The mechanisms for primary hyperalgesia to mechanical stimuli may be both peripheral and central, but the importance of peripheral mechanisms is unclear and central mechanisms may account for mechanical hyperalgesia in both the primary and th
-
Neuroscience letters · May 2000
Involvement of spinal protein kinase C in induction and maintenance of both persistent spontaneous flinching reflex and contralateral heat hyperalgesia induced by subcutaneous bee venom in the conscious rat.
To further study the roles of spinal protein kinase C (PKC) in induction and maintenance of both the persistent spontaneous nociception and the contralateral heat hyperalgesia induced by subcutaneous (s.c.) bee venom injection, the effects of intrathecal (i.t.) treatment with a PKC inhibitor, chelerythrine chloride (CH), were evaluated in conscious rats. Pre-treatment i.t. with CH at three doses of 0.01, 0.1 and 1 nmol produced a dose-dependent suppressive effect on the flinching reflex with the inhibitory rates of 39, 48 and 59%, respectively, when compared with the pre-saline control group. ⋯ Post-treatment i.t. with the drug at the highest dose used (1 nmol) also resulted in a 35% reversal effect on the established contralateral heat hyperalgesia. The present result suggests that activation of PKC in the spinal cord contributes to the induction and maintenance of both peripherally-dependent persistent spontaneous pain and contralateral heat hyperalgesia which is dependent upon central sensitization.
-
Human subjects infected with herpes or varicella-zoster viruses complain of pain, such as allodynia, in or near the region with vesicles. However, the mechanisms of the pain are unclear. We show for the first time that infection with herpes simplex virus type-1 (HSV-1) induces allodynia and hyperalgesia in mice. ⋯ In contrast, when started from days 5 or 6, acyclovir treatment slightly inhibited the development of skin lesions and the viral proliferation, but not allodynia and hyperalgesia. These results suggest that the propagation of HSV-1 in the dorsal root ganglia produces allodynia and hyperalgesia as a result of functional abnormality of the sensory neurons in mice. This may be a useful model for studying the mechanisms of herpetic pain.
-
Randomized Controlled Trial Clinical Trial
Effect of preoperative oral dextromethorphan on immediate and late postoperative pain and hyperalgesia after total abdominal hysterectomy.
Dextromethorphan is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist known to inhibit wind-up and NMDA-mediated nociceptive responses of dorsal horn neurons. Experimental and clinical studies indicate that NMDA-receptor antagonists may potentiate the effect of analgesics such as morphine, local anesthetics and NSAIDs. Results from previous clinical studies of dextromethorphan in postoperative pain are conflicting, possibly related to administration of insufficient doses of the drug. ⋯ There were no significant differences in side-effects (nausea, vomiting, sedation). In conclusion, oral dextromethorphan 150 mg reduced PCA morphine consumption immediately (0-4 h) after hysterectomy, without prolonged effects on pain or wound hyperalgesia. A positive correlation between the magnitude of wound hyperalgesia at 24 h after operation, and total 24 h postoperative PCA morphine consumption was demonstrated.