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Complex Regional Pain Syndrome type 1 (CRPS-1) is a disabling condition characterized by sensory, autonomic, (vaso)motor and trophic disturbances, of which pain, swelling, color changes, limited mobility and change in temperature of the affected extremity are the most predominant [4,33]. CRPS-1 mainly develops after fractures, operations or a small trauma but also occasionally develops without a triggering event [26]. Different mechanisms are thought to play a role in the development of CRPS-1, providing a possible explanation for the heterogeneity seen within this patient population. One of the mechanisms proposed to be involved in the origin and maintenance of CRPS-1 is an exaggerated inflammatory response to tissue injury [2]. Scientific evidence supports the involvement of inflammatory processes in CRPS-1, whereby elevated cytokine levels [17], elevated activity of mast cells, neurogenic inflammatory reactions, [2,18] and markers of oxidative stress [6] were found. Systematic reviews addressing anti-inflammatory therapy provide limited evidence and contradictory conclusions [7,20,27]. However, in recent years additional studies have been published targeting the inflammatory component of CRPS-1. In light of the changing views about the involvement of inflammation, a comprehensive assessment of anti-inflammatory treatment approaches of CRPS-1 is warranted. The goal of the present topical review is to evaluate the effect of anti-inflammatory therapy on prevention, pain, range of motion and overall clinical improvement in CRPS-1.

Terminally ill patients suffering from intractable cancer pain are treated in our hospital on an outpatient basis with a percutaneous intrathecal (i.t.) catheter and a portable pump delivering morphine continuously. In a patient showing an increased demand of morphine the dose was raised from 1.5 to 2 mg/h, but pain intensity did not decrease. Subsequently a 1.5 ml dose of 5% lidocaine was administered; however, no motor or sensory block was observed. After controlling the catheter position and passage through the catheter, a sample of cerebrospinal fluid (CSF) was taken and the pH was measured. It was found to be outside the physiological range of 7.19 (normal range: 7.27-7.37), possibly explaining the decreased activity of the local anesthetic. The purpose of this study was to determine the influence of morphine, with or without sodium metabisulfite, on pH in vitro, using artificial CSF (ACSF) and on pH in vivo during i.t. administration of morphine. An in vitro model was used to measure pH changes by adding a morphine solution (concentrations of 0.5, 2, 5 and 10 mg/ml) with and without sodium metabisulfite to ACSF solutions (Elliott B). Fourteen patients were consecutively selected for continuous administration of morphine. An i.t. catheter was inserted, tunnelled and connected with an external pump (Provider 5500, Abbott, Chicago, IL). CSF was aspirated and pH was measured with a blood-gas system (Ciba-Corning 288, Medfield, USA). In vitro, morphine solutions with or without sodium metabisulfite added to an Elliott B solution (pH = 7.47, 37 degrees C) caused a concentration-related decrease in pH.(ABSTRACT TRUNCATED AT 250 WORDS)