Pain
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Case Reports
Patterns of spread in complex regional pain syndrome, type I (reflex sympathetic dystrophy).
There are reports that complex regional pain syndrome, type I (reflex sympathetic dystrophy; CRPS-I/RSD) can spread from the initial site of presentation, but there are no detailed descriptions of the pattern(s) of such spread. We describe a retrospective analysis of 27 CRPS-I/RSD patients who experienced a significant spread of pain. Three patterns of spread were identified. 'Contiguous spread (CS)' was noted in all 27 cases and was characterized by a gradual and significant enlargement of the area affected initially. 'Independent spread (IS)' was noted in 19 patients (70%) and was characterized by the appearance of CRPS-I in a location that was distant and non-contiguous with the initial site (e.g. ⋯ In some it may be due to a local spread of pathology (CS); in others it may be a consequence of a generalized susceptibility (IS). In the MS case, spread may be due to abnormal neural functioning spreading via commissural pathways. Alternatively, we discuss the possibility that all three kinds of spread may be due to aberrant CNS regulation of neurogenic inflammation.
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Our understanding of the natural history of chronic pain in the community is limited. This is partly due to the lack of a validated measure of chronic pain severity known to be responsive to change over time. The Chronic Pain Grade questionnaire has been shown to be valid and reliable for use in a general population as a self-completion questionnaire. ⋯ The majority of SF-36 scores changed in the hypothesized directions. Changes in CPG scores were significantly correlated with changes in most of the SF-36 domains. We concluded that the CPG is a useful and valid objective instrument for measuring change in severity of chronic pain over time and could be used in longitudinal studies of chronic pain severity.
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Possible role of inflammatory mediators in tactile hypersensitivity in rat models of mononeuropathy.
Peripheral hypersensitivity (hyperalgesia and allodynia) are common phenomena both in inflammatory and in neuropathic pain conditions. Several rat models of mononeuropathy (Bennett, Seltzer and Gazelius models) display such symptoms following partial injury to the sciatic nerve. Using immunohistochemistry and behavioral tests, we investigated inflammatory cell and cytokine responses in the sciatic nerve 14 days after injury created in these different models as well as after axotomy. ⋯ Our findings indicate that the considerable increase in monocytes/macrophages induced by a nerve injury results in a very high release of IL-6 and TNF-alpha. This may relate to the generation of tactile allodynia/hyperalgesia, since there was a clear correlation between the number of ED-1 and IL-6-positive cells and the degree of allodynia. It is possible that measures to reduce monocyte/macrophage recruitment and the release of pro-inflammatory interleukins after nerve damage could influence the development of neuropathic pain.