Articles: hyperalgesia.
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Pain assessment and physical examination are the first crucial steps in diagnosis of neuropathic pain disorders because these are still solely diagnosed on clinical grounds. The physical examination should be conducted in such a way that all of the positive sensory phenomena, such as allodynia, hyperalgesia, hyperpathia, summation, and after-sensation are elicited. Other physical examination findings should corroborate the diagnostic impression of neuropathic pain. Specific pain diagnosis should then lead to more specific therapy.
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Review Randomized Controlled Trial Clinical Trial
Experimental evaluation of the analgesic effect of ibuprofen on primary and secondary hyperalgesia.
The analgesic effect of systemic ibuprofen was investigated with two human experimental pain models: (i) static mechanical stimulation of the inter digital web between the 2nd and 3rd finger and (ii) primary and secondary hyperalgesia induced by a 7-min burn injury on the calf. In each double-blind, randomized, two-way cross-over study 20 healthy male volunteers received either ibuprofen 600 mg or placebo tablets. ⋯ Previous human experimental studies concerning the analgesic effect of NSAIDs are reviewed. Based on the previous literature and the present results we suggest that NSAIDs inhibit progressive tactile hypersensitivity but not the central sensitization itself.
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Review
Interactions of sympathetic and primary afferent neurons following nerve injury and tissue trauma.
Sympathetic post-ganglionic neurons may be involved in the generation of pain, hyperalgesia and inflammation under pathophysiological conditions. Two categories of influence of the sympathetic neuron on afferent neurons can be distinguished and this distinction seems to be related to whether the coupling between afferent and sympathetic neuron develops after nerve lesion or after tissue trauma with inflammation (Fig. 15): A. Peripheral nerve lesion generates plastic changes of the afferent and sympathetic postganglionic neurons, depending on the type of nerve lesion (e.g. complete, partial). ⋯ Sympathetically mediated (neurogenic) inflammation and neurogenic inflammation mediated by afferents may interact reciprocally and enhance the inflammatory process as well as the sensitization of nociceptive afferents. Norepinephrine may also lead to sensitization of nociceptive afferents under inflammatory conditions. This sensitization is presumably mediated by alpha 2-adrenoceptors in the sympathetic varicosities and by a prostaglandin (probably PGI2) which is synthesized and released by or in association with the sympathetic varicosities.
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Ugeskrift for laeger · Jun 1995
Review[Morphine-induced hyperalgesia, allodynia and myoclonus--new side-effects of morphine?].
During the last ten years hyperalgesia (H), allodynia (A) and myoclonia (M) has been reported at an increased frequency in human beings treated with morphine. The side effects are most common in cancer patients treated with high dose morphine, and has been reported for all routes of administration. ⋯ The first mentioned theory is the most likely. The treatment of morphine induced H, A, and M seems to be to discontinue morphine administration and to initiate therapy with other opioids (fentanyl, sufentanyl, methadone or ketobemidone).