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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Meta Analysis
Effectiveness of placebo interventions for patients with non-specific low back pain: a systematic review.
Little is known about the effectiveness of placebo interventions in patients with nonspecific low back pain (LBP). This systematic review assessed the magnitude of the effects of placebo interventions as compared to no intervention in randomized controlled trials (RCTs) including patients with LBP. Embase, MEDLINE (Ovid), and Cochrane CENTRAL databases were searched from inception to December 5, 2019. ⋯ These results show placebo interventions are more effective than no intervention at short-term follow-up in patients with chronic LBP. However, the magnitude of the effects is probably not clinically relevant (approximately 8 points on a 0-100 pain scale). Future research should identify effect modifiers and causal mechanisms explaining the short-term effects of placebo interventions in patients with chronic LBP.
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Observational Study
The responsiveness of quantitative sensory testing-derived sensory phenotype to disease-modifying intervention in patients with entrapment neuropathy: a longitudinal study.
The German Research Network on Neuropathic Pain (DFNS) quantitative sensory testing (QST) method for sensory phenotyping is used to stratify patients by mechanism-associated sensory phenotype, theorised to be predictive of intervention efficacy. We hypothesised that change in pain and sensory dysfunction would relate to change in sensory phenotype. We investigated the responsiveness of sensory phenotype to surgery in patients with an entrapment neuropathy. ⋯ Quantitative sensory testing-derived sensory phenotype is sensitive to clinically important change. In an entrapment neuropathy model, sensory phenotype was associated with patient-reported symptoms and demonstrated statistically significant, clinically relevant change after disease-modifying intervention. Sensory phenotype was independent of disease severity and may reflect underlying neuropathophysiology.
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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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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.