Articles: neuralgia.
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Spinal cord stimulation (SCS) is believed to exert supraspinal effects; however, these mechanisms are still far from fully elucidated. This systematic review aims to assess existing neurophysiological and functional neuroimaging literature to reveal current knowledge regarding the effects of SCS for chronic neuropathic pain on brain activity, to identify gaps in knowledge, and to suggest directions for future research. ⋯ The limited available evidence regarding supraspinal mechanisms of SCS does not allow us to develop any conclusive theories. However, the studies included appear to show an inhibitory effect of SCS on somatosensory evoked potentials, as well as identifying the thalamus and anterior cingulate cortex as potential mediators of the pain experience. The lack of substantial evidence in this area highlights the need for large-scale controlled studies of this kind.
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Changes in the nerve's microenvironment and local inflammation resulting from peripheral nerve injury participate in nerve sensitization and neuropathic pain development. Taking part in these early changes, disruption of the blood-nerve barrier (BNB) allows for infiltration of immunocytes and promotes the neuroinflammation. However, molecular mechanisms engaged in vascular endothelial cells (VEC) dysfunction and BNB alterations remain unclear. ⋯ In vitro, activation of Toll-like receptor 4 in VEC downregulated the components of Hh pathway and altered the endothelial functional state. Inhibition of Hh signaling in the ScN of naive rats mimicked the biochemical and functional alterations observed after CCI and was, on its own, sufficient to evoke local neuroinflammation and sustained mechanical allodynia. Alteration of the Hh signaling pathway in VEC associated with peripheral nerve injury, is involved in BNB disruption and local inflammation, and could thus participate in the early changes leading to the peripheral nerve sensitization and, ultimately, neuropathic pain development.
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Annals of neurology · Apr 2016
Randomized Controlled TrialBotulinum toxin type A for neuropathic pain in patients with spinal cord injury.
To evaluate the analgesic effect of botulinum toxin type A (BTX-A) on patients with spinal cord injury-associated neuropathic pain. ⋯ These results indicate that BTX-A may reduce intractable chronic neuropathic pain in patients with spinal cord injury.
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A range of outcome measures across various domains are used to evaluate change following an intervention in clinical trials on chronic neuropathic pain (NeP). However, to capture a real change in the variable of interest, the psychometric properties of a particular measure should demonstrate appropriate methodological quality. Various outcome measures in the domains of pain and physical functioning have been used in the literature for NeP, for which individual properties (eg, reliability/validity) have been reported. To date, there is no definitive synthesis of evidence on the psychometric properties of those outcome measures; thus, the aim of this systematic review was to evaluate the methodological quality [COnsensus-based Standards for the selection of health status Measurement INstruments (COSMIN) guidelines] of studies that evaluated psychometric properties of pain and physical functioning outcome measures used for NeP. ⋯ Although a variety of pain and physical functioning outcome measures have been reported in the literature, few have demonstrate methodologically strong psychometric properties. Thus, future research is required to further investigate the psychometric properties of existing pain and physical functioning outcome measures used for clinical and research purposes.
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J. Pharmacol. Exp. Ther. · Apr 2016
The Selective Monoacylglycerol Lipase Inhibitor MJN110 Produces Opioid-Sparing Effects in a Mouse Neuropathic Pain Model.
Serious clinical liabilities associated with the prescription of opiates for pain control include constipation, respiratory depression, pruritus, tolerance, abuse, and addiction. A recognized strategy to circumvent these side effects is to combine opioids with other antinociceptive agents. The combination of opiates with the primary active constituent of cannabis (Δ(9)-tetrahydrocannabinol) produces enhanced antinociceptive actions, suggesting that cannabinoid receptor agonists can be opioid sparing. ⋯ This combination did not reduce gastric motility or produce subjective cannabimimetic effects in the drug discrimination assay. Importantly, combinations of MJN110 and morphine given repeatedly (i.e., twice a day for 6 days) continued to produce antiallodynic effects with no evidence of tolerance. Taken together, these findings suggest that MAGL inhibition produces opiate-sparing events with diminished tolerance, constipation, and cannabimimetic side effects.