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Post-thoracotomy pain syndrome (PTPS) develops after a thoracotomy (open or laparoscopic) and is one of the most often reported chronic postsurgical pain syndromes.

Pain is transmitted to the central nervous system via thinly myelinated Aδ and unmyelinated C-fibers. The former convey the sensation of sharp, lancinating “first” pain, whereas the latter conduct the dull, longer-lasting “second” pain. Aδ-fibers predominantly respond to mechanical stimuli (Type I or “high-threshold mechanoreceptor”) or to noxious heat (Type II). Conversely, the C-fibers are polymodal, the same fiber responding to mechanical, thermal and chemical stimuli. Both Aδ- and C-fibers terminate in the superficial dorsal horn, mainly in Rexed Laminae I and II, although some Aδ-fibers also terminate in the deeper lamina V. In the periphery, the distal endings terminate freely in the tissues. These free nerve endings express a variety of signal transducing molecules, one of the most extensively investigated being the transient receptor potential ion channel TRPV1, also known as the capsaicin receptor [1].

Phantom Limb Pain (PLP) is the feeling of pain in a limb, portion of a limb, or organ after its amputation. PLP can also occur after nerve avulsions or spinal cord injuries. Around 80 % of people who undergo amputation experience some degree of PLP.

Spinal cord stimulation (SCS) is a treatment option for severe neuropathic pain not responsive to more conservative treatments. Common indications include FBSS, CRPS types 1 and 2, and painful radiculopathies. Other indications include but are not limited to painful peripheral vascular disease, post-herpetic neuralgia, and axial low back pain. Careful patient selection is paramount; contraindications include but are not limited to certain severe psychological comorbidities, active infection, and an inability to pause anticoagulants for the procedure. Prior to implantation of the impulse generator, the patient must first undergo a trial with a percutaneous or surgically placed lead and show at least a 50 % improvement in pain or functional status.

The intercostal nerve block (ICN) is used in acute and chronic pain conditions of the thorax and the upper abdomen. It can be performed for analgesia in cases of rib fractures or in chronic pain conditions such as postmastectomy and post-thoracotomy pain.

Background Inadequately treated postoperative pain can lead to longer healing processes, longer hospital stays and the development of chronic pain. In a 900-bed university hospital in Switzerland pain scores were assessed systematically. The study's primary aim was to define whether the routine pain assessment on the ward is accurate and reproducible. Subsequently the obtained data were used for a benchmark analysis to determine the hospitals performance in pain assessment quality compared with similar centers. Methods During a 3-month period PAIN OUT questionnaires were used for patients’ interviews. Patients were included randomly according to the daily surgical schedule. Pain scores were assessed routinely by nursing staff on the wards and compared to PAIN OUT data. The ascertained data was analyzed by descriptive statistics as well as the Wilcoxon test for non parametric values using IBM SPSS. Results 658 patients were included in the study. Comparing routine pain measurements with PAIN OUT results revealed that within the first 24 hours on the ward pain scores were significantly lower than measured with PAIN OUT questionnaires. This difference increased with increasing pain scores. The quality of pain management of the hospital in which this study was performed ranged around the fiftieth percentile when compared to similar centers. Conclusion The cross sectional data comparison of pain assessment by the ward staff and by interviews with the PAIN OUT questionnaire showed a large gap of underrated pain. The benchmark analysis with the method of PAIN OUT suggests a decent pain management among reference groups. This article is protected by copyright. All rights reserved.

AIMS: The aim of this present study was to investigate the changes of peripheral sensory nerve excitability produced by propofol. MAIN METHODS: In a recently described in vitro model of rodent saphenous nerve we used the technique of threshold tracking (QTRAC®) to measure changes of axonal nerve excitability of Aβ-fibres caused by propofol. Concentrations of 10μMol, 100μMol and 1000μMol were tested. Latency, peak response, strength-duration time constant (τSD) and recovery cycle of the sensory neuronal action potential (SNAP) were recorded. KEY FINDINGS: Our results have shown that propofol decreases nerve excitability of rat primary sensory afferents in vitro. Latency increased with increasing concentrations (0μMol: 0.96±0.07ms; 1000μMol 1.10±0.06ms, P

Contrasting findings have been published regarding the role of magnesium sulphate used as an additive to local anaesthetics in peripheral nerve blocks.To clarify the effect of magnesium sulphate on nerve excitability.C and Aβ compound action potentials were recorded extracellularly in vitro in saphenous nerves from adult rats.Saphenous nerves (n = 30) from male Wistar rats (n = 19), 12 to 16 weeks old.Primary sensory afferents were tested with a computerised threshold tracking program (QTRAC) with a supramaximal 1 ms current pulse either alone or after 300 ms of conditioning polarising ramp currents in the presence and absence of 10 mmol l magnesium sulphate, 80 μmol l lidocaine and a combination of both.Changes in current thresholds to elicit compound action potential amplitudes of 40% of the maximal response.Magnesium sulphate increased excitability thresholds to a greater extent in Aβ fibres than in C fibres. It enhanced the effects of lidocaine in both Aβ fibres [mixture 0.470 mA (SD 0.105) versus lidocaine 0.358 mA (SD 0.080), P0.001] and C fibres [mixture 2.531 mA (SD 0.752) versus lidocaine 2.385 mA (SD 0.656), P = 0.008]. Preconditioning experiments also showed that magnesium sulphate had an enhancing effect with lidocaine in Aβ fibres [mixture 0.620 mA (SD 0.281) versus lidocaine 0.543 mA (SD 0.315), P = 0.005], but not in C fibres [mixture 2.412 mA (SD 0.641), lidocaine 2.461 mA (SD 0.693), P = 0.17].These results suggest that the binding of magnesium ions depends on both the type and conformational state of voltage-gated sodium channels. They also may help to explain the conflicting reports regarding the clinical effects of magnesium sulphate as an additive to lidocaine in peripheral nerve blocks.

OBJECTIVES: The conformational state of voltage-gated sodium channels is an important determinant for the efficacy of both local anesthesia and electrical neuromodulation techniques. This study investigated the role of subthreshold preconditioning ramp currents on axonal nerve excitability parameters in the presence of sodium channel blockers in myelinated A and unmyelinated C fibers. MATERIALS AND METHODS: A- and C-fiber compound action potentials were recorded extracellularly in vitro in saphenous nerve from adult rats. Nerve fibers were stimulated with a supramaximal current pulse either alone or after a 300-msec conditioning polarizing ramp current (between -10% and +100% of the original threshold current) in the presence and absence of lidocaine and tetrodotoxin (TTX). A computerized threshold tracking program (QTRAC(©) , Institute of Neurology, University College London, London, UK) was used to determine the membrane thresholds. RESULTS: Preconditioning ramp currents of weak strengths increased membrane excitability. Stronger preconditioning ramp currents enhanced the potency of lidocaine and TTX to increase excitability thresholds. In A and C fibers stimulated with ramp currents of 110% (A fibers) and 40% (C fibers), lidocaine (80 μM) induced a 168 ± 15% (p < 0.001) and 302 ± 23% (p < 0.001) increase in threshold, respectively (no ramp current: 135 ± 9% and 124 ± 4%, respectively). TTX (16 nM) induced an increase in threshold of 455 ± 45% (p < 0.001) and 214 ± 22% (p = 0.005), respectively (no ramp current: 205 ± 12% and 128 ± 6%, respectively). CONCLUSIONS: Slow preconditioning ramp stimuli inactivate sodium currents. In the presence of sodium channel blockers, stronger ramp stimuli cause an increase in threshold, which is larger than that caused by the sodium channel blocker alone. Therefore, we conclude that small depolarizing ramp currents could be used to increase excitability threshold in the presence of low concentrations of local anesthetics. These additive effects might represent a target to address with peripheral nerve stimulation in order to suppress afferent pain signaling.