Articles: hyperalgesia.
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To determine perception and pain thresholds in patients with fibromyalgia syndrome and in healthy controls, and to investigate whether patients with fibromyalgia syndrome can be grouped with respect to thermal hyperalgesia and whether these subgroups differ from healthy controls and in clinical appearance. ⋯ Patients with fibromyalgia syndrome were subgrouped by quantitative sensory testing (i.e., thermal pain thresholds). Subgroups show clinical differences in pain intensities, number of tender points, and sleep quality. Cold pain threshold was especially linked to these clinical aspects.
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Previous studies have established that the activation of peripheral nociceptors alters the central processing of nociceptive stimuli. In this study, we examined whether noxious heating of the dental pulp enhances the nociceptive jaw-opening reflex (JOR) and the expression of the immediate early gene c-fos in chloral hydrate/pentobarbital-anesthetized ferrets. We hypothesized that the application of noxious heat to the dental pulp, a procedure that evokes a preferential activation of pulpal C-fibers, will enhance JOR responses to electrical stimulation of the tooth pulp and that this enhanced response will be associated with the expression of Fos protein in discrete regions of the trigeminal nucleus. ⋯ The enhancement in JOR responses was independent of temporal summation of the electrical stimulus for test stimuli delivered at either 1.0 or 0.1 Hz. Sensitization of the JOR was associated with an increase in the number of immunohistochemically identified Fos-positive nuclei in trigeminal caudalis (Vc) and the transition zone between trigeminal interpolaris and caudalis (Vi/Vc) ipsilateral to the site of stimulation compared with sham stimulated animals. These findings suggest that neuronal populations in Vc and Vi/Vc play a role in the enhanced reflex responses to tooth pulp stimulation and may contribute to the pain and hyperalgesia associated with a symptomatic pulpitis.
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In a previous study we demonstrated that injection (i.p.) of low doses of GM1 ganglioside in mice rapidly attenuates morphine's analgesic effects. This result is consonant with our electrophysiologic studies in nociceptive types of dorsal root ganglion (DRG) neurons in culture, which showed that exogenous GM1 rapidly increased the efficacy of excitatory (Gs-coupled) opioid receptor functions. By contrast, treatment of DRG neurons with the non-toxic B-subunit of cholera toxin (CTX-B) which binds selectively to GM1, blocked the excitatory, but not inhibitory, effects of morphine and other bimodally-acting opioid agonists, thereby resulting in a net increase in inhibitory opioid potency. ⋯ These results are comparable to the effects of cotreatment of mice with morphine plus an ultra-low dose of the opioid antagonist, naltrexone (NTX) which blocks opioid-induced hyperalgesic effects, unmasking potent opioid analgesia. Low-dose NTX selectively blocks excitatory opioid receptors at their recognition site, whereas CTX-B binds to, and interferes with, a putative allosteric GM1 regulatory site on excitatory opioid receptors. Furthermore, chronic cotreatment of mice with morphine plus CTX-B attenuates development of opioid tolerance and physical dependence, as previously shown to occur during cotreatment with low-dose NTX.
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Comparative Study
Histamine-induced itch converts into pain in neuropathic hyperalgesia.
Physiologically, itch and pain are transmitted in separate specific peripheral C-units and central afferent pathways. Some neuropathic pain patients with intact but sensitized (irritable) primary C-nociceptors have spontaneous pain, heat hyperalgesia, static and dynamic mechanical hyperalgesia. The question was whether cutaneous histamine application induces pain in these patients. ⋯ Itch was profoundly inhibited. Conversely, histamine application in neuropathic skin induced severe increase in spontaneous burning pain but no itch. In neuropathies irritable nociceptors may express histamine receptors or induce central sensitization to histaminergic stimuli so that itch converts into pain.
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Anesthesia and analgesia · Nov 2001
Systemic tizanidine hydrochloride (Zanaflex) relieves thermal hyperalgesia in rats with an experimental mononeuropathy.
We sought to determine whether tizanidine, an alpha2-agonist, relieved thermal hyperalgesia in rats with surgically induced neuropathic pain. We used a Sprague-Dawley rat model in which a chronic constriction of the sciatic nerve caused the rats to develop postural changes, mechanical allodynia, and thermal hyperalgesia. Thermal hyperalgesia was verified through paw withdrawal latency (PWL). PWL was tested before surgery, after surgery, and after injections with tizanidine (0.5, 1.0, or 2.0 mg/kg) or normal saline. Ambulatory and total movements were evaluated by placing the rats in activity cages. Thermal hyperalgesia was induced in all rats after surgery. Tizanidine, but not saline, caused a significant improvement in PWL (P < 0.05), with complete reversal of thermal hyperalgesia at all doses on postoperative Day 6. Rats who received tizanidine 2 mg/kg maintained complete reversal of thermal hyperalgesia through postoperative Day 9. Some sedation was observed with tizanidine 2 mg/kg, but not with smaller doses. We conclude that tizanidine effectively reversed thermal hyperalgesia in a rat model. ⋯ This study was conducted to determine whether tizanidine could attenuate the thermal hyperalgesia that occurs in rats with surgically induced chronic constriction of the sciatic nerve. Tizanidine was effective in reducing sensitivity to heat, as measured by paw withdrawal latency, and did not cause sedation at smaller doses.