Articles: hyperalgesia.
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Comparative Study Clinical Trial
The impact of ethnic differences in response to capsaicin-induced trigeminal sensitization.
Ethnic differences in the experience of pain, pain-related health care utilization and pain-reducing activities have been reported. Thus, evaluating of such variations is important in clinical and experimental pain. Since clinical pain is greatly influenced by disease-specific factors (severity, duration, type and treatment), evaluating ethnic differences in experimental pain models may not only provide some information about underlying mechanisms but also may predict or explain group differences in clinical pain. ⋯ Pain sensitivity, secondary hyperalgesic area, and pressure pain threshold were assessed. Overall, the model showed significant greater pain responses in South Indians (8.75+/-1.25 cm pain intensity and 9.33+/-2.32 cm2 hyperalgesic area) compared to Caucasians (6.25+/-1.95 cm pain intensity and 6.25+/-1.41 cm2 hyperalgesic area). The model may provide important information for further clinical research, e.g. migraine or differences in mechanisms underlying trigeminal sensitization.
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Anesthesia and analgesia · Sep 2005
The antiallodynic and antihyperalgesic effects of neurotropin in mice with spinal nerve ligation.
Although Neurotropin(R) (NTP) has been used clinically as an analgesic in Japan for many years, its effect on neuropathic pain in animal models has not been examined in detail. Its main effect has been indicated to be activation of the descending monoaminergic pain inhibitory systems. To study the effect of NTP on neuropathic pain, we subjected mice to spinal nerve ligation. ⋯ When the effect of NTP was examined after depletion of monoamines in the spinal cord by intrathecal neurotoxins, the antiallodynic and antihyperalgesic effects were still observed after serotonergic denervation, but not after noradrenergic denervation. In addition, intracerebroventricular NTP increased withdrawal threshold and latency although intrathecal or local administration of NTP did not. These results suggest that the antiallodynic and antihyperalgesic effect of NTP on neuropathic pain induced by spinal nerve ligation is mediated principally through the action at supraspinal sites and through activation of spinal noradrenergic systems, possibly via the descending inhibitory pathway.
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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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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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This study examined the differences in tactile hypersensitivity across 6 different strains of male mice, and between male and female rats of 3 different strains in a rodent model of low back pain associated with lumbar radiculopathy. ⋯ Different mouse strains, and male and female rats that are exposed to identical nerve root injuries have diverse levels of tactile hypersensitivity, supporting the hypothesis that genetic factors and sex play a key role in radicular pain. Our results correlate with data compiled in identical mouse and rat strains after L5-L6 nerve ligation, suggesting that the precise nature of the injury is not relevant to the inheritance of neuropathic symptom sensitivity.