Articles: function.
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Total knee arthroplasty (TKA) is one of the most performed surgical operations in the United States. Managing postoperative pain after TKA is of vital importance, as it is positively associated with outcome measures related to recovery of function and quality of life. Two commonly used methods to control postoperative pain are regional anesthesia (RA), consisting of a single or a combination of peripheral nerve and epidural blocks, and pain medication, such as opioids. Our retrospective analysis sought to better understand whether revision versus primary TKA impacted previously discovered disparities in perioperative pain management and use of RA at the Atlanta Veterans Affairs Health Care System (AVAHCS). Before data collection, we hypothesized that revision TKA would have a higher proportion of Black and older patients and that revision TKA patients would have lower postoperative pain scores. ⋯ Sociodemographic disparities in pain management have been reported in all healthcare systems, including the VAHCS. This moderately sized retrospective study, conducted at a single veterans affairs site, yielded several noteworthy findings. One finding of particular interest was that, despite Black patients reporting higher baseline and 24-hour postoperative pain scores, they were prescribed fewer opioids at discharge. Our results highlight the presence of clinically significant disparities in perioperative TKA pain management, emphasizing the need for continuous investigation and focused mitigation efforts among Veterans.
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The 2 tetrodotoxin-resistant (TTXr) voltage-gated sodium channel subtypes NaV1.8 and NaV1.9 are important for peripheral pain signaling. As determinants of sensory neuron excitability, they are essential for the initial transduction of sensory stimuli, the electrogenesis of the action potential, and the release of neurotransmitters from sensory neuron terminals. NaV1.8 and NaV1.9, which are encoded by SCN10A and SCN11A, respectively, are predominantly expressed in pain-sensitive (nociceptive) neurons localized in the dorsal root ganglia (DRG) along the spinal cord and in the trigeminal ganglia. ⋯ Successful knockout of both channels was verified by whole-cell recordings demonstrating the absence of NaV1.8- and NaV1.9-mediated Na+ currents in NaV1.8/NaV1.9 DKO DRG neurons. Global RNA sequencing identified significant deregulation of C-LTMR marker genes as well as of pain-modulating neuropeptides in NaV1.8/NaV1.9 DKO DRG neurons, which fits to the overall only moderately impaired acute pain behavior observed in DKO mice. Besides addressing the function of both sodium channels in pain perception, we further demonstrate that the null-background is a very valuable tool for investigations on the functional properties of individual human disease-causing variants in NaV1.8 or NaV1.9 in their native physiological environment.
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Stroke is the second-leading cause of death worldwide. OSA is an independent risk factor for stroke and is associated with multiple vascular risk factors. Poststroke OSA is prevalent and closely linked with various stroke subtypes, including cardioembolic stroke and cerebral small vessel disease. Observational studies have shown that untreated poststroke OSA is associated with an increased risk of recurrent stroke, mortality, poorer functional recovery, and longer hospitalizations. ⋯ There is a need for high-quality randomized controlled trials in poststroke OSA that may provide evidence to support the utility of CPAP (and/or other treatment modalities) in reducing recurrent vascular events and mortality. This goal may be achieved by examining treatment strategies that have yet to be trialed in poststroke OSA, tailoring interventions according to poststroke OSA endotypes and phenotypes, selecting high-risk populations, and using metrics that reflect the physiologic abnormalities that underlie the harmful effects of OSA on cardiovascular outcomes.