Pain
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Compared with racism and sexism, classism in pain assessment and management practices (PAMPs) has been less investigated, and its mediating mechanisms are still unknown. Drawing on a social psychological model of dehumanization, this research aimed to test (1) the effect of patient socioeconomic status (SES; a proxy of social class) on PAMPs and (2) whether patient dehumanization and perceived life hardship mediated these effects. Two online experimental studies were conducted, in which patient SES was manipulated (low vs high) within-subjects. ⋯ Patient mechanistic dehumanization mediated SES effects on pain disability (medical students alone). Perceived life hardship mediated SES effects on pain disability, credibility (nurses alone), and intentions of providing individualized care (nurses alone). These finding bear novel contributions to the fields of pain, health service research, and social psychology and have important implications to the development of more effective future interventions to reduce classism in PAMPs.
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Pain is a complex experience that involves sensation, emotion, and cognition. The subjectivity of the traditional pain measurement tools has expedited the interest in developing neuroimaging techniques to monitor pain objectively. Among noninvasive neuroimaging techniques, functional near-infrared spectroscopy (fNIRS) has balanced spatial and temporal resolution; yet, it is portable, quiet, and cost-effective. ⋯ Starting from the experimental design, we reviewed the regions of interest, probe localization, data processing, and primary findings of these existing fNIRS studies. We also discussed the fNIRS imaging's potential as a brain surveillance technique for pain, in combination with artificial intelligence and extended reality techniques. We concluded that fNIRS is a brain imaging technique with great potential for objective pain assessment in the clinical environment.
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Dorsal root ganglion field stimulation (GFS) relieves evoked and spontaneous neuropathic pain by use-dependent blockade of impulse trains through the sensory neuron T-junction, which becomes complete within less than 1 minute for C-type units, also with partial blockade of Aδ units. We used this tool in the spinal nerve ligation (SNL) rat model to selectively block sensory neuron spontaneous activity (SA) of axotomized neurons at the fifth lumbar (L5) level vs blockade of units at the L4 level that remain uninjured but exposed to inflammation. In vivo dorsal root single-unit recordings after SNL showed increased SA in L5 units but not L4 units. ⋯ In addition, L5 GFS, but not L4 GFS, increased mechanical threshold of DH units during cutaneous mechanical stimulation, while L5 GFS exceeded L4 GFS in reducing evoked firing rates. Our results indicate that SA in injured neurons supports increased firing of DH wide-dynamic-range neurons, contributing to hyperalgesia, allodynia, and ongoing pain. Ganglion field stimulation analgesic effects after nerve injury are at least partly attributable to blocking propagation of this SA.
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Tricyclic antidepressants that inhibit serotonin and noradrenaline reuptake, such as amitriptyline, are among the first-line treatments for neuropathic pain, which is caused by a lesion or disease affecting the somatosensory nervous system. These treatments are, however, partially efficient to alleviate neuropathic pain symptoms, and better treatments are still highly required. Interactions between neurons and glial cells participate in neuropathic pain processes, and importantly, connexins-transmembrane proteins involved in cell-cell communication-contribute to these interactions. ⋯ Another connexin blocker, carbenoxolone, also improved amitriptyline action. Additional in vitro studies suggested that mefloquine may also directly act on serotonin transporters and on adenosine A1 and A2A receptors, but drugs acting on these other targets failed to amplify amitriptyline action. Together, our data indicate that pharmacological blockade of connexins potentiates the therapeutic effect of amitriptyline in neuropathic pain.
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Accumulating evidence suggests hippocampal impairment under the chronic pain phenotype. However, it is unknown whether neuropathic behaviors are related to dysfunction of the hippocampal circuitry. Here, we enhanced hippocampal activity by pharmacological, optogenetic, and chemogenetic techniques to determine hippocampal influence on neuropathic pain behaviors. ⋯ Altogether, these results imply that downregulation of the DH circuitry during chronic neuropathic pain aggravates pain-related behaviors. Conversely, activation of the DH reverses pain-related behaviors through local excitatory and opioidergic mechanisms affecting DH functional connectivity. Thus, this study exhibits a novel causal role for the DH but not the VH in controlling neuropathic pain-related behaviors.