Articles: hyperalgesia.
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The activity of nefopam, a centrally acting compound, not structurally related to other analgesics, was examined in acute and postoperative thermal pain models in the rat. Its antinociceptive potency was evaluated using heat noxious stimuli either in intact or in injured animals after skin and muscular incisions. In the hot plate and in the plantar tests, nefopam after acute administration by different routes exhibited a dose-dependent attenuation of the nociceptive responses at 10-30 mg x kg(-1) by intraperitoneal or subcutaneous administration, at 60 mg x kg(-1) by oral dosing, and from 3 mg x kg(-1) after intravenous injection. ⋯ In the same conditions, morphine and tramadol displayed antinociceptive activities. As the plantar test provides a good index of nociception in humans, these results point out the usefulness of nefopam for attenuating moderate to severe pain, and for postoperative analgesia. In conclusion, nefopam has shown potent properties to reduce thermal hypersensitivity after acute or postoperative pain in rats.
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J. Pediatr. Hematol. Oncol. · Dec 2001
Case ReportsLong-term treatment with ketamine in a 12-year-old girl with severe neuropathic pain caused by a cervical spinal tumor.
A 12-year-old girl presented with head and neck pain, myoclonic movements, and decreased strength in all extremities caused by a cervical spinal tumor (glioblastoma multiforme). A partial resection of the tumor was performed. Three weeks later, she had superficial pain distributed in all dermatomes below her cervical medullary lesion. ⋯ For the last 29 days of life, the pain treatment regimen was successfully continued in her home (400-km distance from the hospital). In conclusion, this case demonstrates that ketamine treatment may be effective in children with severe neuropathic pain not responsive to other analgesics. This patient also demonstrates the feasibility of long-term ketamine treatment in pediatric oncology and that such treatment can be administered in a home care setting.
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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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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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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.