Articles: neuropathic-pain.
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Emerging lines of evidence indicate that production of reactive oxygen species (ROS) at distinct sites of the nociceptive system contributes to the processing of neuropathic pain. However, the mechanisms underlying ROS production during neuropathic pain processing are not fully understood. We here detected the ROS-generating nicotinamide adenine dinucleotide phosphate oxidase isoform Nox2 in macrophages of dorsal root ganglia (DRG) in mice. ⋯ Nox2-deficient mice displayed reduced neuropathic pain behavior after peripheral nerve injury, whereas their immediate responses to noxious stimuli were normal. Moreover, injury-induced upregulation of tumor necrosis factor α was absent, and activating transcription factor 3 induction was reduced in DRG of Nox2-deficient mice, suggesting an attenuated macrophage-neuron signaling. These data suggest that Nox2-dependent ROS production in macrophages recruited to DRG contributes to neuropathic pain hypersensitivity, underlining the observation that Nox-derived ROS exert specific functions during the processing of pain.
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Evaluation of nociceptive sensitisation in canine osteoarthritis studies has been poorly reported, or even related to other clinical symptoms. In 16 dogs, peak vertical force (PVF), subjective pain assessment using 3 scales, sympathetic stress response with electrodermal activity (EDA) measurement, and behavioural changes with video analysis and telemetered motor activity were quantified at baseline (D-7), and 28 and 56 days post transection of the cranial cruciate ligament. As markers of central sensitisation, selected spinal cord biomarkers (substance P and transthyretin) were quantified at D56. ⋯ Compared to tiludronate, at D56, vehicle-treated dogs had increased spinal substance P (P=0.01), concomitant decreased transthyretin (P=0.02), and (compared to baseline) demonstrated peripheral and central QST sensitisation, which was not present for tiludronate. Only PVF, the spontaneous behaviour "walking with full weight-bearing," and EDA were associated with occurrence of QST sensitisation and indicated significant tiludronate analgesic efficacy after inclusion of central QST sensitisation as a predictor variable in the statistical model. This study establishes the strong interest to implement QST as a predictor of canine osteoarthritis pain symptoms explained by pain sensitisation.
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Spinal cord stimulation (SCS) is well accepted for the treatment of chronic pain since its beginning in 1967. As its use continues to enter into the chronic pain treatment algorithm earlier, conscience patient selection and durability of the therapy are clearly clinically relevant. To improve treatment efficacy, consensus statements and guidelines were developed. ⋯ The current available guideline statements have clear deficiencies in either scope of coverage, evidence synthesis, or lack of transparency of funding. Improved evidence and best practice/guideline assessment may improve patient outcomes and accessibility to these important modalities. Further prospective comparator randomized data are required to not only provide data of clinical and cost-effectiveness in other indications but also to better describe the position of neurostimulation application within the disease management pathway. Therein cases where there appears to be sufficient evidence and consensus, every effort should be made to secure access to these effective therapies. Importantly, each guideline only has a useful clinical half-life, if not updated. This should be acknowledged by both clinicians and third-party payers. Based on these deficiencies, the International Neuromodulation Society recommended the creation of a consensus conference to examine the appropriate use of neurostimulation for pain and ischemic disease.
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Background and aims We have previously reported that systemic administration of sinomenine produced antinociception in various experimental pain conditions in rodents, particularly in models of neuropathic pain. In the present study we assessed the effects of repeated administration of sinomenine in two rodent models of neuropathic pain in order to study the development of tolerance. Methods The analgesic effect of sinomenine was tested in female Sprague-Dawley rats that exhibited mechanical and cold hypersensitivity following ischaemic injury to the spinal cord and in male C57/BL6 mice that developed mechanical hypersensitivity after ischaemic injury to the sciatic nerve. ⋯ The effect of sinomenine on response threshold persisted for days after termination of the 5 day drug administration. Conclusions The results suggest that repeated administration of simomenine produced an enhanced anti-allodynic effect without tolerance in rodent models of neuropathic pain. Implications Sinomenine may be tested as a novel analgesic in treating some forms of chronic neuropathic pain in patients.
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Current data suggest that transcranial magnetic stimulation (TMS) has the potential to be an effective and complimentary treatment modality for patients with chronic neuropathic pain syndromes. The success of TMS for pain relief depends on the parameters of the stimulation delivered, the location of neural target, and duration of treatment. TMS can be used to excite or inhibit underlying neural tissue that depends on long-term potentiation and long-term depression, respectively. Long-term randomized controlled studies are warranted to establish the efficacy of repetitive TMS in patients with various chronic pain syndromes.