Neuroimmune alterations in the complex regional pain syndrome

Department of Anaesthesiology, Erasmus University Medical Centre Rotterdam, Dijkzigt Hospital, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands
European Journal of Pharmacology (Impact Factor: 2.53). 11/2001; 429(1-3):101-113. DOI: 10.1016/S0014-2999(01)01310-3
Source: PubMed


This review focuses on some clinical aspects of the complex regional pain syndrome, such as oedema, local temperature changes and chronic pain, as a result of supposed neurogenic inflammation. Involvement of the immune system could imply the subsequent release of neuropeptides, pro-inflammatory cytokines and eicosanoids, which in turn leads to a complex cross-talk of primary and secondary generated mediators of inflammation. The development and application of drugs that act through selective receptor antagonism or enzymatic synthesis inhibition to prevent further stimulation of this cascade that could inevitably lead to chronicity of this disease are extensively discussed.

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    • "Nerve growth factor is one of the cytokines activated by the substance P, and its activity leads to nociceptive sensitization, enhanced osteopenia with increased cytokine content (Sabsovich et al., 2008). Tumor necrosis factor alpha is another pro-inflammatory cytokine postulated to play a role in the development of CRPS changes after trauma and its expression is increased in CRPS patients (Huygen et al., 2001). Although the increased level of the tumor necrosis factor is an important mediator of regional nociceptive sensitization, it does not contribute to the enhanced bone loss (Sabsovich et al., 2008). "
    Osteoporosis, 02/2012; , ISBN: 978-953-51-0026-3
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    • "Complex regional pain syndrome (CRPS) refers to a chronic pain condition associated with autonomic disturbances of vasomotor and sudomotor origin (1), along with trophic skin changes and patchy demineralization of the bones (2). Although the mechanism for CRPS has not been elucidated, studies indicate that it is a complex disorder involving both the central and peripheral nervous systems (3, 4). This complex etiology of CRPS is manifested by its heterogeneous constellation of clinical symptoms. "
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    ABSTRACT: We evaluated the efficacy of oral alendronate with different dosing regimens for non-nociceptive symptoms and osteoporosis in a sciatic nerve chronic constriction injury (CCI) model. Male Sprague-Dawley rats (n=60) were subdivided into sham control (SC) group and CCI groups, which were divided according to dosage and time of oral alendronate administration: no treatment (NT), low dosage early (LE), high dosage early (HE), low dosage late (LL) and high dosage late (HL). We measured the thickness and temperature of the hind paw, bone mineral density (BMD) of the tibia, along with tibia bone strength. On the 14th day post-CCI, the HE group showed significant reduction in thickness and temperature (P<0.001). On the 42nd day post-CCI, the HE group showed significant reduction in temperature compared to the NT group (P<0.001). Also, both HE and HL groups showed statistically significant increased tibia BMD (P<0.001), along with increase of tibia bone strength compared to the NT group. Based on these findings, early alendronate in high dosages is effective in the non-nociceptive symptoms; early and late alendronate in high dosages, are effective in preventing bone dystrophic changes in a CCI model.
    Journal of Korean medical science 06/2010; 25(6):938-44. DOI:10.3346/jkms.2010.25.6.938 · 1.27 Impact Factor
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    • "In general, three mechanisms are thought to be involved: afferent mechanisms (e.g., neurogenic inflammation) [2–4], efferent mechanisms (e.g., autonomic disturbances) [5], and central nervous system mechanisms (e.g., cerebral plasticity) [6]. Based on our review of the literature regarding the CRPS pathophysiology, we hypothesized that following a trauma or surgery, the normal sterile inflammatory response runs out of control, and is perhaps initiated by a genetic and/or acquired immunologic disorder [7]. Neuroimmune activation of cells in the peripheral nervous system, which is part of the afferent mechanism, apparently results in central sensitization and exacerbation of pain [8]. "
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    ABSTRACT: In an earlier study, levels of the proinflammatory cytokines TNF-alpha and IL-6 are higher in blisters fluid from the complex regional pain syndrome type 1 (CRPS1) side obtained at 6 and 30 months (median) after the initial event. The aim of this follow-up study is to determine the involvement of these cytokines in long lasting CRPS1. Twelve CRPS1 patients, with median disease duration of 72 months, participated. The levels of TNF-alpha and IL-6 were measured in blister fluid; disease activity was reevaluated by measuring pain and differences in temperature, volume, and mobility between both extremities. Differences in levels of IL-6 and TNF-alpha and mobility between both sides were significantly decreased. Pain and differences in temperature and volume were not significantly altered. No correlation was found between the cytokines and the disease characteristics. These results indicate that IL-6 and TNF-alpha are only partially responsible for the signs and symptoms of CRPS1.
    Mediators of Inflammation 02/2008; 2008:469439. DOI:10.1155/2008/469439 · 3.24 Impact Factor
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