Spinal cord stimulation for chronic pain of neuropathic or ischaemic origin: systematic review and economic evaluation. (41/114)

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Systemic inflammatory mediators in post-traumatic complex regional pain syndrome (CRPS I) - longitudinal investigations and differences to control groups. (42/114)

OBJECTIVES: The Complex Regional Pain Syndrome I (CRPS I) is a disease that might affect an extremity after trauma or operation. The pathogenesis remains yet unclear. It has clinical signs of severe local inflammation as a result of an exaggerated inflammatory response but neurogenic dysregulation also contributes to it. Some studies investigated the role inflammatory mediators and cytokines; however, few longitudinal studies exist and control groups except healthy controls were not investigated yet. METHODS: To get further insights into the role of systemic inflammatory mediators in CRPS I, we investigated a variety of pro-, anti-, or neuro-inflammatory mediators such as C-Reactive Protein (CRP), White Blood Cell Count (WBC), Interleukins 4, 6, 8, 10, 11, 12 (p70), Interferon gamma, Tumor-Necrosis-Factor alpha (TNF-a) and its soluble Receptors I/II, soluble Selectins (E,L,P), Substance-P (SP), and Calcitonin Gene-Related Peptide (CGRP) at different time points in venous blood from patients with acute (AC) and chronic (CC) CRPS I, patients with forearm fractures (FR), with neuralgia (NE), and from healthy volunteers (C). RESULTS: No significant changes for serum parameters investigated in CRPS compared to control groups were found except for CC/C (CGRP p = 0.007), FR/C (CGRP p = 0.048) and AC/CC (IL-12 p = 0.02; TNFRI/II p = 0.01; SP p = 0.049). High interindividual variations were observed. No intra- or interindividual correlation of parameters with clinical course (e.g. chronification) or outcome was detectable. CONCLUSION: Although clinically appearing as inflammation in acute stages, local rather than systemic inflammatory responses seem to be relevant in CRPS. Variable results from different studies might be explained by unpredictable intermittent release of mediators from local inflammatory processes into the blood combined with high interindividual variabilities. A clinically relevant difference to various control groups was not notable in this pilot study. Determination of systemic inflammatory parameters is not yet helpful in diagnostic and follow-up of CRPS I.  (+info)

Post-junctional facilitation of Substance P signaling in a tibia fracture rat model of complex regional pain syndrome type I. (43/114)

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The role of enhanced cutaneous IL-1beta signaling in a rat tibia fracture model of complex regional pain syndrome. (44/114)

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Development of Korean Academy of Medical Sciences guideline-rating the impairment in pain. (45/114)

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Complex regional pain syndrome type 1 and scurvy. (46/114)

A 5 year old female developed features of complex regional pain syndrome (CRPS) i.e excessive pain to touch, decreased sweating and edema of left ankle 2 years after fracture of left tibia. Gum bleeding, petechiae and pseudoparalysis and suggestive radiograph characterized scurvy. Hyperesthesia improved and child walked with support following administration of vitamin C.  (+info)

Complex regional pain syndrome type I: efficacy of stellate ganglion blockade. (47/114)

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Evidence based guidelines for complex regional pain syndrome type 1. (48/114)

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