Articles: hyperalgesia.
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Objective. Development of a spinal cord stimulation (SCS) system in a mouse model of chronic neuropathic pain. Materials and Methods. Male C57BL/6 mice (N = 6) underwent a partial ligation of the sciatic nerve. Development of mechanical hyperalgesia was tested using the withdrawal response to tactile stimuli with the von Frey test. ⋯ After termination of the SCS, the withdrawal threshold of the ipsilateral paw slowly decreased. No effect of SCS on the contralateral paw was noted. Conclusion. The development of a mouse SCS system is described that is practical in use, is reproducible, and shows a comparative therapeutic effect in treatment of chronic neuropathic pain as reported in rat.
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J Pain Symptom Manage · Oct 2007
Clinical TrialManaging the symptoms of neuropathic pain: an exploration of patients' experiences.
The debilitating effects of chronic neuropathic pain on everyday life are considerable, but little is known about how individual sufferers manage these effects. Virtually nothing is known about what patients prefer, what measures they take themselves and when, or in what combinations. The aim of this study was to explore patients' reports of how they managed their neuropathic pain symptoms. ⋯ Some had tried to accept their pain, but there was insufficient psychological, social, emotional, and practical support to allow them to do this successfully. This exploratory study provides a basis from which to develop a larger study to validate and extend the findings. Other issues meriting research are the effectiveness of cognitive-behavioral therapies for those with neuropathic pain, and an exploration and subsequent evaluation of different types of social, practical, and emotional support needed to help live with neuropathic pain.
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The neurobiologic basis of pancreatic hyperalgesia in chronic pancreatitis (CP) is understood poorly and there is a need to identify novel therapeutic targets. Our aim was to study the role of the transient receptor potential vanilloid 1 (TRPV1), a key integrator of noxious stimuli, in the pathogenesis of pancreatic pain in a rat model of CP. ⋯ TRPV1 up-regulation and sensitization is a specific molecular mechanism contributing to hyperalgesia in CP and represents a useful target for treating pancreatic hyperalgesia caused by inflammation.
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Randomized Controlled Trial
Mechanisms of adrenosensitivity in capsaicin induced hyperalgesia.
It is well known that iontophoresis of norepinephrine in capsaicin treated skin is followed by an increase in thermal hyperalgesia. It is unclear if this action on nocicepitive afferents involves the release of prostaglandins. The aim of the present study was to determine: (1) the effect of norepinephrine iontophoresis on spontaneous and evoked pain in the human skin after topical application of capsaicin; (2) the effect of cyclooxygenase (COX) inhibition on changes in pain perception induced by norepinephrine application. ⋯ The results do not support the assumption that in human skin sensitized by topical capsaicin application of norepinephrine acts on nociceptive afferents via the release of prostaglandins. Thus, a direct action of norepinephrine on adrenergic receptors in the membrane of the afferent fibers is most likely.
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Acta Anaesthesiol Scand · Oct 2007
Randomized Controlled Trial Comparative StudyMethylprednisolone and ketorolac rapidly reduce hyperalgesia around a skin burn injury and increase pressure pain thresholds.
Glucocorticoids and non-steroidal anti-inflammatory drugs (NSAIDs) decrease acute postoperative pain and hyperalgesia. The objectives of this study were to investigate the effects of methylprednisolone and ketorolac on hyperalgesia around a skin burn injury and on pressure pain thresholds. ⋯ Methylprednisolone and ketorolac increased PPTT attenuated secondary hyperalgesia around a skin burn injury. PPTT increased after both methylprednisolone and ketorolac. The present study demonstrates analgesic and anti-hyperalgesic properties of a glucocorticoid and a non-selective NSAID that have not been demonstrated previously in human subjects.