Articles: neuralgia.
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Review Meta Analysis
Should non-pharmacological and non-surgical interventions be used to manage neuropathic pain in adults with spinal cord injury? - a systematic review.
Spinal Cord Injury (SCI) results in a permanent or temporary alteration of the motor, sensory and/or autonomic functions, frequently leading to neuropathic pain. To deal with this comorbidity, several non-pharmacological and non-surgical (NP-NS) interventions have been developed. However, their efficacy is still uncertain. ⋯ Further studies with homogeneous protocols and methodological quality are still needed. PERSPECTIVE: This article presents a review of existing studies on the effectiveness of NP-NS interventions in neuropathic pain in SCI. This synthesis could potentially alert and motivate clinicians to develop studies on this topic, so that interventions can be objectively evaluated and recommendations for an evidence-based practice be created.
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We previously established a macaque model of central post-stroke pain (CPSP) and confirmed the involvement of increased activity of the posterior insular cortex (PIC) and secondary somatosensory cortex (SII) to somatosensory stimuli in mechanical allodynia by a combination of imaging techniques with local pharmacological inactivation. However, it is unclear whether the same intervention would be effective for thermal hyperalgesia. Therefore, using the macaque model, we examined behavioural responses to thermal stimuli following pharmacological inactivation of the PIC/SII. ⋯ CPSP is caused by stroke lesions in the sensory system and characterized by mechanical allodynia or thermal hyperalgesia. Inactivation of the PIC/SII has an analgesic effect on mechanical allodynia; however, it is not clear whether the same intervention could reduce thermal hyperalgesia. Here, using the macaque model, we demonstrated that inactivation of these cortices reduces hypersensitivity to thermal stimuli. This result emphasizes that increased PIC/SII activity can contribute to abnormal pain of multiple modalities.
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This article reviews PTPS demographics, diagnosis, pathophysiology, surgical and anesthetic techniques, and their role in preventing PTPS along with updated treatment options. ⋯ Post-thoracotomy pain syndrome (PTPS) can be incapacitating. The neuropathic type pain of PTPS is along the incision site and persists at least 2 months postoperatively. There is a wide reported range of prevalence of PTPS. There are several risk factors that have been identified including surgical technique and younger age. Several surgical and anesthetic techniques have been trialed to reduce pain after thoracotomy. Multimodal pain control is the suggested long-term treatment plan for patients with PTPS. There are several factors that can be modified to reduce pain and incidence of PTPS during the perioperative period and the use of multimodal analgesia is suggested for the treatment of PTPS.
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Experimental studies have suggested that nitrous oxide-induced analgesia depends on interactions with opioids. On the basis of these results, we hypothesized that the effects of inhaled nitrous oxide/oxygen (N 2 O/O 2 ) 50%-50% equimolar mixture (EMONO) on patients with neuropathic pain would be higher in those receiving concomitant opioids. To test this hypothesis, we did exploratory post hoc analyses of our recently published ProtoTOP study to compare the effects of EMONO and placebo in patients with or without concomitant opioid treatment. ⋯ The proportion of patients with at least 30% pain reduction and of those reporting an overall improvement with the Patient Global Impression of Change were significantly higher only in this population of patients. In conclusion, these results complement our previous analyses with the identification of a specific population of responders to EMONO inhalation in patients with neuropathic pain. As suggested by experimental studies, we hypothesized that these long-lasting analgesic effects could depend on the anti-N-methyl-D-aspartate properties of N 2 O.
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Intrathecal application of contulakin-G (CGX), a conotoxin peptide and a neurotensin analogue, has been demonstrated to be safe and potentially analgesic in humans. However, the mechanism of action for CGX analgesia is unknown. We hypothesized that spinal application of CGX produces antinociception through activation of the presynaptic neurotensin receptor (NTSR)2. ⋯ Anatomical studies demonstrated coexpression of NTSR2 and Cav2.3 in dorsal root ganglion neurons. Finally, synaptic fractionation and slice electrophysiology recordings confirmed a predominantly presynaptic effect. Together, these data reveal a nonopioid pathway engaged by a human-tested drug to produce antinociception.