Articles: hyperalgesia.
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In view of the paucity of studies on central poststroke pain (CPSP), in this hospital-based prospective study, we evaluated the frequency, the spectrum, imaging, and quantitative sensory testing in a cohort of stroke patients with CPSP. ⋯ CPSP was present in 20.7% of the stroke patients. Spinothalamic tract dysfunction may not be necessary for the development of CPSP, and it can also be seen with normal spinothalamic sensation. The location of the stroke, its type and quality, and the severity of CPSP were not related.
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Int J Psychophysiol · Nov 2016
Randomized Controlled TrialExpectation of nocebo hyperalgesia affects EEG alpha-activity.
Changes in EEG activity have been related to clinical and experimental pain. Expectation of a negative outcome can lead to pain enhancement (nocebo hyperalgesia) and can alter the response to therapeutic interventions. The present study characterizes EEG alteration related to pain facilitation by nocebo. ⋯ Five-minute EEG was recorded under: resting state, tonic innocuous heat and tonic noxious heat before and after the application of a sham inert cream to the non-dominant volar forearm combined with cognitive manipulation. The intensity and unpleasantness of heat-induced pain increased after cognitive manipulation in the nocebo group compared to control and was associated with enhanced low alpha (8-10Hz) activity. However, changes in alpha activity were predicted by catastrophizing but not by pain intensity or unpleasantness, which suggest that low alpha power might reflect brain activity related to negative cognitive-affective responses to pain.
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Chronic inflammatory and peripheral neuropathic pain (PNP) is a major health problem for which effective drug treatment is lacking. The pathophysiology of these debilitating conditions is incompletely understood, but nerve growth factor (NGF) is believed to play a major role. NGF-antagonism has previously been shown to prevent pain hypersensitivity in rodent models of acute inflammatory pain and PNP, but most of those animal studies did not address the more clinically relevant issue of whether NGF-antagonism provides relief of established chronic pain behavior. Therefore, the aim of this study was to investigate whether blocking NGF actions with a humanized anti-NGF monoclonal antibody (PG110) would reverse/attenuate established pain hypersensitivity in rat models of chronic/persistent inflammatory pain and PNP. ⋯ These findings suggest that therapies that target NGF or its receptors may be effective for treatment of persistent/chronic inflammatory pain, but probably not PNP.
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Crotalphine is a structural analogue to a novel analgesic peptide that was first identified in the crude venom from the South American rattlesnake Crotalus durissus terrificus. Although crotalphine's analgesic effect is well established, its direct mechanism of action remains unresolved. The aim of the present study was to investigate the effect of crotalphine on ion channels in peripheral pain pathways. ⋯ Likewise, crotalphine acted on peptidergic TRPA1-expressing nerve endings ex vivo as demonstrated by suppression of calcitonin gene-related peptide release from the trachea and in vivo by inhibition of chemically induced and inflammatory hypersensitivity in mice. The crotalphine-mediated desensitizing effect was abolished by the TRPA1 blocker HC030031 and absent in TRPA1-deficient mice. Taken together, these results suggest that crotalphine is the first peptide to mediate antinociception selectively and at subnanomolar concentrations by targeting TRPA1 ion channels.
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Randomized Controlled Trial
Low-dose butorphanol alleviates remifetanil-induced hyperalgesia in patients undergoing laparoscopic cholecystectomy.
To evaluate the effects of low-dose butorphanol on hyperalgesia induced by high-dose remifetanil in patients undergoing laparoscopic cholecystectomy. ⋯ A high dose of remifentanil induces postoperative hyperalgesia, which could be prevented by a continuous intravenous administration of a low dose of butorphanol.