Spinal cord stimulation in the treatment of complex regional pain syndrome type 1: Is trial truly required?

OBJECTIVE: Spinal cord stimulation has been proven highly effective in the treatment of Complex Regional Pain Syndrome (CRPS). The definitive implantation of a neurostimulator is usually preceded by a therapeutic test (trial), which has the purpose of identifying whether the patient would respond positively to neuromodulation or not. The present study aims to analyze the surgical results of spinal cord stimulation in type 1 CRPS patients who have not undergone trial. PATIENTS AND METHODS: From January 2011 to August 2017, 160 patients underwent implantation of spinal cord neurostimulator. Out of that total number of surgeries, 33 patients were unequivocally diagnosed with type 1 Complex Regional Pain Syndrome and selected for this study. The efficacy of the surgical procedure concerning pain improvement was analyzed through the application of the Pain Disability Index and the Visual Analog Pain Scale. RESULTS: The mean sample age was 48.08 years. The majority of the study subjects were female (66.66%). In respect to the Pain Disability Index, a 65% improvement in disability was observed subsequently to the neurostimulator implantation; in addition, the means of the scores for preoperative and postoperative periods were, respectively, 55 ±â€¯8.69 (p < 0.0001) and 18.90 ±â€¯11.58 (p < 0.0001). Regarding the Visual Analogue Scale, the mean pain in the preoperative period was 9.43 ±â€¯0.77 (p < 0.0001), while the mean in postoperative period was 2.86 ±â€¯2.08 (p < 0.0001). Thus, an average reduction of 70% of painful symptoms was observed after the surgical procedure. CONCLUSION: Implantation of a spinal cord neurostimulator presented significant improvement in pain and disability of patients with type 1 CRPS in all cases. These results were obtained following the criteria: 1) patients presenting unequivocal diagnosis of type 1 CRPS; 2) submitted to constant current spinal cord neurostimulator implant; 3) underwent intraoperative tests for precise location of the spinal cord electrode implantation. Therefore, it is possible to suggest that a trial may be unnecessary in that subgroup of patients. Further studies would be required to confirm these findings.

The effect of d-galactose induced oxidative stress on in vitro redox homeostasis in rat plasma and erythrocytes.

We, herein, investigated the in vitro effects of galactose on thiobarbituric acid-reactive substances (TBA-RS), total sulfhydryl content, and on the activities of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and butyrylcholinesterase (BuChE) in the blood of 30- and 60-day-old rats. We also determined the influence of the antioxidants, trolox, ascorbic acid and glutathione, on the effects elicited by galactose on the parameters tested. Galactose was added to the assay at final concentrations of 0.1, 3.0, 5.0 and 10.0mM. Control experiments were performed without the addition of galactose. Rats were sacrificed by decapitation without anesthesia and a blood sample was removed for analysis. Galactose, at 3.0mM, 5.0mM and 10.0mM, enhanced TBA-RS in the plasma of 60-day-old rats, while 10.0mM galactose reduced total sulfhydryl content in the plasma of 30-day-old rats; 5.0mM and 10.0mM galactose enhanced CAT activity in the erythrocytes of 30- and 60-day-old rats and 10.0mM galactose reduced SOD activity in the erythrocytes of 60-day-old rats. Galactose did not alter BuChE activity. Data showed that at the pathologically high concentration (greater than 5.0mM), galactose induces lipid peroxidation, reduces total sulfhydryl content and alters antioxidant defenses in the blood of rats. Trolox, ascorbic acid and glutathione addition prevented most alterations in oxidative stress parameters that were caused by galactose. Our findings lend support to a potential therapeutic strategy for this disease, which may include the use of antioxidants for ameliorating the damage caused by galactose.