Spinal cord stimulation for chronic non-cancer pain: a review of current evidence and practice

Spinal cord stimulation provides analgesia through electrical stimulation of the dorsal column of the spinal cord via electrode leads placed into the epidural space. In traditional tonic stimulation, a painful sensation is replaced with paraesthesia. Spinal cord stimulation is effective in reducing neuropathic pain, enhancing function, and improving quality of life in different chronic pain conditions. Currently, there is most evidence to support its use for failed back surgery syndrome when multidisciplinary conventional management is unsuccessful. Temporary trial leads are inserted in carefully selected patients to test their responsiveness prior to permanent implantation. Newer neuromodulation modalities are now available. These include burst stimulation, high-frequency stimulation, and dorsal root ganglion stimulation. Results are encouraging to date, and they may provide superior analgesia and cover for deficiencies of traditional tonic stimulation. Although complications are not uncommon, they are rarely life threatening or permanently disabling. Nonetheless, device removal is occasionally needed.link_to_OA_fulltex

Efficacy of Pregabalin in Acute Postoperative Pain Under Different Surgical Categories: a meta-analysis

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Effects of Intra-Operative Total Intravenous Anaesthesia with Propofol versus Inhalational Anaesthesia with Sevoflurane on Post-Operative Pain in Liver Surgery: A Retrospective Case-Control Study

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The Legacy of Leaded Gasoline in Bottom Sediment of Small Rural Reservoirs

The historical and ongoing lead (Pb) contamination caused by the 20th-century use of leaded gasoline was investigated by an analysis of bottom sediment in eight small rural reservoirs in eastern Kansas, USA. For the reservoirs that were completed before or during the period of maximum Pb emissions from vehicles (i.e., the 1940s through the early 1980s) and that had a major highway in the basin, increased Pb concentrations reflected the pattern of historical leaded gasoline use. For at least some of these reservoirs, residual Pb is still being delivered from the basins. There was no evidence of increased Pb deposition for the reservoirs completed after the period of peak Pb emissions and (or) located in relatively remote areas with little or no highway traffic. Results indicated that several factors affected the magnitude and variability of Pb concentrations in reservoir sediment including traffic volume, reservoir age, and basin size. The increased Pb concentrations at four reservoirs exceeded the U.S. Environmental Protection Agency threshold-effects level (30.2 mg kg-1) and frequently exceeded a consensus-based threshold-effects concentration (35.8 mg kg-1) for possible adverse biological effects. For two reservoirs it was estimated that it will take at least 20 to 70 yr for Pb in the newly deposited sediment to return to baseline (pre-1920s) concentrations (30 mg kg-1) following the phase out of leaded gasoline. The buried sediment with elevated Pb concentrations may pose a future environmental concern if the reservoirs are dredged, the dams are removed, or the dams fail

An audit of changes in outcomes of acute pain service: evolution over the last two decades

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Propofol produces preventive analgesia via GluN2B-containing NMDA Receptor/ERK1/2 Signaling Pathway in the rat model of Inflammatory Pain

Compared to other anesthetics, propofol has showed superior analgesic effect used during surgical procedures on acute post-surgical pain. Whether propofol has preventive analgesic property remain debated. The present study investigated the antinociceptive effect of propofol and underlying molecular and cellular mechanisms via pre-emptive administration in a formalin-induced inflammatory pain model in rats. Male adult Sprague-Dawley rats were randomly allocated into 4 groups: naïve (Group Naïve), formalin injection only (Group Formalin), and formalin injection at 30 min (Group P-30min) or 2 h (Group P-2h) after intravenous infusion of propofol (0.6 mg kg-1 min-1) for 1 h. Nociceptive responses were evaluated by composite pain score-weighted scores. Protein expression of phosphorylated- or pan-GluN2B, ERK1/2, p38 MAPK and JNK in the spinal dorsal horn was assessed by Western blot. Alteration of intracellular Ca2+ concentration induced by NMDA receptor agonists with or without pre-treatment of propofol was measured using fluorometry in SH-SY5Y cells. Neuronal activation was assessed by immunofluorescence. Pre-emptive propofol reduced pain with a delayed response to formalin and a reduction in hypersensitivity that lasted at least for 2 h. The formalin-induced activation of spinal GluN2B and ERK1/2 but not p38 or JNK were also diminished by propofol treatment. Preconditioning treatment with 3 µM and 10 µM of propofol inhibited Ca2+ influx mediated through NMDA receptors in SH-SY5Y cells. Propofol also reduced the neuronal expression of c-Fos and p-ERK induced by formalin. These findings indicate that pre-emptive administration of propofol produces preventive analgesic effects on inflammatory pain through regulating neuronal GluN2B-containing NMDA receptor and ERK1/2 pathway in the spinal dorsal horn.published_or_final_versio