Articles: hyperalgesia.
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The present studies were conducted to examine functional consequences of postnatal chronic inflammation, initiated during a critical developmental period, on capsaicin-evoked hyperalgesia and neuronal activation in adulthood. Rats received a unilateral intraplantar injection of complete Freund's adjuvant (CFA; diluted 2:1 in saline) on postnatal day 0 (P0-CFA) or 14 (P14-CFA). Separate groups received an equivalent volume of saline on P0 (P0-vehicle) or were untreated (P0-untreated). Increases in capsaicin-evoked thermal and mechanical hyperalgesia and allodynia were observed in adult P0-CFA-treated rats relative to control conditions. By contrast, this enhancement was absent in P14-CFA-treated rats, suggesting that the developmental period differentially affects the appearance of the observed behavioral phenotype. Capsaicin-evoked nocifensive behavior was also lower in P14-CFA-treated rats relative to P0-CFA-treated rats. Capsaicin-evoked Fos protein expression was increased in the superficial and neck regions of the dorsal horn of adult P0-CFA-treated rats relative to P0-vehicle-treated rats. These changes were absent in the nucleus proprius and ventral horn. The present data are consistent with the hypothesis that neonatal chronic inflammation permanently alters sensitivity to pain in adulthood, consistent with modulation of primary afferent activation and central sensitization in response to a subsequent nociceptive challenge in adulthood. ⋯ Chronic inflammation during development can induce profound alterations in sensory processing later in life. Here we show that long-term inflammation initiated at critical developmental stages sensitizes both behavioral and neuronal responses to nociceptor stimulation in adulthood. An ongoing sensitization of the spinal cord is induced by the postnatal inflammatory insult.
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Neuropathic pain can be both ongoing or stimulus-induced. Stimulus-induced pain, also known as hyperalgesia, can be differentiated into primary and secondary hyperalgesia. The former results from sensitization of peripheral nociceptive structures, the latter involves sensitization processes within the central nervous system (CNS). ⋯ Interestingly, stronger activations of GC, contralateral MFC and anterior insula significantly correlated to higher ratings of the stimulus-related unpleasantness. We conclude that thermal and mechanical hyperalgesia produce substantially different brain activation patterns. This is linked to different psychophysical properties.
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Anesthesia and analgesia · Dec 2005
Spinal L-type calcium channel blockade abolishes opioid-induced sensory hypersensitivity and antinociceptive tolerance.
Recent studies have suggested that prolonged exposure to morphine results in the development of paradoxical, abnormal enhanced pain. It has also been suggested that this enhanced pain state may be interpreted as antinociceptive tolerance. Although the precise mechanisms that drive opioid-induced abnormal pain are not well known, considerable evidence suggests that this state may be supported by enhanced, stimulus-evoked excitatory transmission. ⋯ These hypersensitivities were prevented by the coadministration of the putative selective L-type calcium channel blocker amlodipine. Moreover, mice receiving morphine for 8 days demonstrated a significant rightward shift of the morphine antinociceptive dose-response curve, indicative of antinociceptive tolerance, whereas those that also received amlodipine along with morphine did not demonstrate tolerance. These results suggest that blockade of the L-type calcium channels with amlodipine prevented opioid-induced hyperalgesia and the expression of antinociceptive tolerance to spinal morphine, presumably by reducing stimulus-induced excitatory neurotransmitter release.
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Transgenic overexpression of NMDA NR2B receptors in forebrain regions increased behavioral responses to persistent inflammatory pain. However, it is not known whether inflammation leads to the upregulation of NR2B receptors in these regions. ⋯ Inhibition of NR2B receptors in the ACC selectively reduced behavioral sensitization related to inflammation. Our results demonstrate that the upregulation of NR2B receptors in the ACC contributes to behavioral sensitization caused by inflammation.
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The gradual development of cutaneous allodynia during the course of a migraine attack is commonly detected by quantitative sensory testing (QST) in migraineurs seeking secondary and tertiary medical help. In this study, the authors developed a questionnaire that tested the recollection of the patients on their skin sensitivity during past migraine attacks. ⋯ The reliability of the questionnaire as a diagnostic tool of allodynia varies with the proportion of allodynic patients in a given clinic. The major source of variability is the misconception of nonallodynic patients that their skin is hypersensitive during migraine.