Articles: hyperalgesia.
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Curr Pain Headache Rep · Dec 2009
ReviewEnhanced pain perception in rheumatoid arthritis: novel considerations.
Enhanced pain perception is common among patients with rheumatoid arthritis (RA). Given the putative role of proinflammatory cytokines in the development of hyperalgesia, a greater understanding of factors that facilitate increased cytokine expression in RA stands to increase understanding of the sources of enhanced pain perception. Patients with RA have significantly greater stress-induced proinflammatory cytokine release. ⋯ Parasympathetic insufficiency has also been demonstrated, which may enhance pain perception indirectly through disinhibited cytokine expression. Several psychological variables have also been demonstrated to affect pain perception in patients with RA. Identification of factors that contribute to enhanced pain perception in RA may aid in the development of novel analgesic strategies that, in turn, may decrease disease activity and improve general clinical outcomes.
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Several studies reported a decreased pain sensitivity in patients with depression, but the underlying neurobiological mechanisms of this phenomenon are unclear. While there is extensive evidence that the serotoninergic system plays a key role in pain modulation, especially in pain inhibitory mechanisms via descending pathways, as well as in the pathophysiology of depression, no study so far has examined its potential relevance in mediating the alteration of pain processing. The present study addresses the question of whether indices of serotoninergic dysfunction, as investigated by a neuroendrocine challenge paradigm, are related to pain sensitivity. ⋯ No such group differences were found with regard to somatosensory thresholds, measures of pain complaints and mood. Subgrouping on the basis of prolactin responsiveness did not reveal significant differences in any parameter. In summary, a decreased pain sensitivity was demonstrated in patients characterized by a reduced neuroendocrine responsiveness to clomipramine, suggesting an involvement of serotoninergic dysfunction underlying altered pain perception in depression.
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The baroreceptor reflex buffers autonomic changes by decreasing sympathetic activity and increasing vagal activity in response to blood pressure elevations, and by the reverse actions when the blood pressure falls. Because of the many bidirectional interactions of pain and autonomic function, we investigated the effect of painful nerve injury by spinal nerve ligation (SNL) on heart rate (HR), blood pressure (BP) and their regulation by the baroreceptor reflex. Rats receiving SNL were separated into either a hyperalgesic group that developed sustained lifting, shaking and grooming of the foot after plantar punctate nociceptive stimulation by pin touch or a group of animals that failed to show this hyperalgesic behavior after SNL. ⋯ The animals that failed to develop hyperalgesia after SNL were found to have elevations in HR both before and for the first 4 days after SNL, and HR variability analysis gave indications of decreased vagal control of resting HR and elevated sympatho-vagal balance at these same time intervals. In human patients, other research has shown that blunted baroreceptor reflex sensitivity predicts poor outcome during conditions such as hypertension, congestive heart failure, myocardial infarction, and stroke. If baroreceptor reflex suppression is also found in human subjects during chronic neuropathic pain, this may adversely affect survival.
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The aim of this study was to investigate tactile sensitivity near the site of primary hyperalgesia evoked by capsaicin applied topically to the dorsolateral aspect of the hand. In the first experiment (N = 15), touch thresholds increased in the fifth finger ipsilateral to the topically applied capsaicin, but remained unchanged at greater distances from the site of capsaicin treatment. In a second experiment (N = 12), the effect of the capsaicin treatment on sensations evoked not only by light touch but also by warmth, heat-pain, and pressure-pain to a 2-mm diameter steel probe was investigated in the fifth finger. ⋯ However, sensitivity to pressure-pain increased in the fifth finger after the capsaicin treatment, possibly due to activation of nociceptors sandwiched between the probe tip and bone that normally responded to sharp stimuli. These findings suggest that the central mechanisms that mediate secondary mechanical hyperalgesia suppress sensitivity to innocuous tactile sensations. This effect may contribute to tactile hypoesthesia in chronic pain conditions.
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Am J Hosp Palliat Care · Nov 2009
Case ReportsBuprenorphine for neuropathic pain--targeting hyperalgesia.
Opioids are well known to relieve severe, acute, and chronic nociceptive pain, but neuropathic pain shows a relatively poor response to opioids. Buprenorphine, a partial mu and ORL-1-receptor agonist, kappa-delta receptor antagonist, interacts with different G proteins than potent mu agonists and hence is not cross-tolerant to standard opioids. ⋯ We present a patient with neuropathic pain and tactile allodynia in which buprenorphine alleviated the hyperalgesia to a greater extent than pain severity. We found buprenorphine to be effective in reducing hypersensitivity in neuropathic pain when pure mu agonists fail to produce a response or in individuals who are intolerant to pure mu agonists.