Articles: hyperalgesia.
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Clinical Trial
Secondary heat hyperalgesia detected by radiant heat stimuli in humans: evaluation of stimulus intensity and duration.
Diverging observations on secondary hyperalgesia to heat stimuli have been reported in the literature. No studies have investigated the importance of heat stimulus intensity and duration for the assessment of secondary heat hyperalgesia. ⋯ The stimulus conditions were systematically varied between three intensity levels (0.8, 1.0 and 1.2 x heat pain threshold (PT)) and four duration steps (200, 350, 500 and 750 ms). The present study shows that long duration (350-750 ms) and low intensity (0.8 and 1.0 x PT) radiant heat stimuli were adequate to detect secondary heat hyperalgesia.
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Br J Clin Pharmacol · Sep 2005
Oral opioid administration and hyperalgesia in patients with cancer or chronic nonmalignant pain.
Previous research has reported on reduced paw withdrawal latencies to heat and mechanical stimuli after parenteral administration of opioids in animals and on increased pain sensitivity in humans subsequent to postoperative infusions of short-acting opioids or in drug addicts. The aim of the present study was to explore the possibility that oral opioid treated patients with cancer-related or chronic nonmalignant pain differ in their pain sensitivity from patients treated with non-opioid analgesics. ⋯ These results suggest that the administration of 'commonly used' dosages of oral opioids does not result in abnormal pain sensitivity beyond that of patients receiving non-opioid analgesia.
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Cold hyperalgesia is a well-documented symptom of inflammatory and neuropathic pain; however, the underlying mechanisms of this enhanced sensitivity to cold are poorly understood. A subset of transient receptor potential (TRP) channels mediates thermosensation and is expressed in sensory tissues, such as nociceptors and skin. Here we report that the pharmacological blockade of TRPA1 in primary sensory neurons reversed cold hyperalgesia caused by inflammation and nerve injury. ⋯ Conversely, intrathecal injection of NGF, but not glial cell line-derived neurotrophic factor, increased TRPA1 in DRG neurons through the p38 MAPK pathway. Together, these results demonstrate that an NGF-induced TRPA1 increase in sensory neurons via p38 activation is necessary for cold hyperalgesia. Thus, blocking TRPA1 in sensory neurons might provide a fruitful strategy for treating cold hyperalgesia caused by inflammation and nerve damage.
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The involvement of the peripheral opioid system in modulating inflammatory pain has been well documented. This study aimed to investigate the possibility of electroacupuncture (EA)-mediated peripheral opioid release. Rats were injected with complete Freund's adjuvant in one of the hind paws to induce localized inflammatory pain. ⋯ Intraplantar but not intraperitoneal injection of naloxone methiodide, a peripherally acting opioid receptor antagonist, eliminated the analgesic effect at 30 minutes after EA treatment. Intraplantar injection of an antibody against beta-endorphin and a corticotropin-releasing factor antagonist also produced a reduction in PWL in rats receiving EA. These data strongly suggest that peripheral opioids are released by EA at the inflammatory site.
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The aim of the study was to determine the frequency of clinical allodynia, osmophobia and red ear syndrome in a young population. Medical records of the children admitted for headache between 1 December 2004 and 31 March 2005 were consecutively studied. A questionnaire was used to find the prevalence of allodynia, osmophobia and red ear syndrome. ⋯ We classified migraine in 57%, other primary headaches in 25% and secondary headaches in about 18%. The presence of ipsilateral clinical allodynia was 14.5% in migraine, osmophobia in 20% of migraine and red ear syndrome in about 24% of migraine cases and they were absent in the other two headache groups. Our study shows that features like osmophobia, allodynia and red ear syndrome are not uncommon in migraine while they are absent in other types of headache.