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To investigate the region-specific effects of painful trigeminal capsaicin stimulation in healthy participants.
Learn More >Despite growing evidence of significant racial disparities in the experience and treatment of chronic pain, the mechanisms by which these disparities manifest have remained relatively understudied. The current study examined the relationship between past experiences of racial discrimination and pain-related outcomes (self-rated disability and depressive symptomatology), and tested the potential mediating roles of pain catastrophizing and perceived injustice related to pain. Analyses consisted of cross-sectional path modeling in a multiracial sample of 137 individuals with chronic low back pain (Hispanics N=43; Blacks N=43; Whites N=51). Results indicated a positive relationship between prior discriminatory experiences and severity of disability and depressive symptoms. In mediation analyses, pain-related appraisals of injustice, but not pain catastrophizing, were found to mediate these relationships. Notably, the association between discrimination history and perceived injustice was significantly stronger in Black and Hispanic participants and was not statistically significant in White participants. The findings suggest that race-based discriminatory experiences may contribute to racial disparities in pain outcomes and highlight the specificity of pain-related, injustice-related appraisals as a mechanism by which these experiences may impair physical and psychosocial function. Future research is needed to investigate temporal and causal mechanisms suggested by the model through longitudinal and clinical intervention studies. PERSPECTIVE: More frequent prior experiences of racial discrimination are associated with greater depressive symptomatology and pain-related disability in individuals with chronic low back pain. These associations are explained by the degree of injustice perception related to pain, but not pain catastrophizing, and were stronger among Black and Hispanic participants.
Learn More >Acupuncture is a complementary and nonpharmacological intervention that can be effective for the management of chronic pain in addition to or instead of medication. Various animal models for neuropathic pain, inflammatory pain, cancer-related pain, and visceral pain already exist in acupuncture research. We used a newly validated human pain model and examined whether acupuncture can influence experimentally induced dental pain. For this study, we compared the impact of manual acupuncture (real acupuncture), manual stimulation of a needle inserted at non-acupuncture points (sham acupuncture) and no acupuncture on experimentally induced dental pain in thirty-five healthy men who were randomized to different sequences of all three interventions in a within-subject design. BORG CR10 pain ratings and autonomic responses (electrodermal activity and heart rate variability) were investigated. An initial mixed model with repeated measures included preintervention pain ratings and the trial sequence as covariates. The results showed that acupuncture was effective in reducing pain intensity when compared to no acupuncture (β =-0.708, p = 0.002), corresponding to a medium Cohen's d effect size of 0.56. The comparison to the sham acupuncture revealed no statistically significant difference. No differences in autonomic responses between real and sham acupuncture were found during the intervention procedures. Perspective: This study established a dental pain model for acupuncture research and provided evidence that experimentally induced dental pain can be influenced by either real acupuncture or manual stimulation of needles at non-acupuncture points. The data do not support that acupoint specificity is a significant factor in reducing experimental pain. Trial registration: The study was registered at clinicaltrials.gov (registration ID: NCT02589418).
Learn More >Glutamate is a neurotransmitter present in most excitatory synapses in the nervous system. It also plays a key role in the spinal cord's physiological excitatory circuit and is involved in pathological neurotransmissions such as those observed in inflammatory and neuropathic pain conditions. The actions of glutamate are mediated by different types of ionotropic (iGluRs) and metabotropic (mGluRs) receptors. Although expressions of iGluRs are well studied, those of mGluRs are not fully elucidated in the spinal cord. In this study, we examined the expressions of mGluRs (mGluR1-8) and investigated which mGluR subtypes can modulate pain transmission in the dorsal horn of the spinal cord using an inflammatory pain model. Reverse transcription-polymerase chain reaction revealed that mGluR mRNAs, except for mGluR2 and 6 mRNAs, were detected in the spinal cord. Double labeling analysis, in situ hybridization histochemistry with immunohistochemistry, was used to examine the distribution of each mGluR in neurons or glial cells in the lamina I-II of the spinal dorsal horn. mGluR1, 5, and 7 were generally, and 4 and 8 were frequently, expressed in neurons. mGluR3 was expressed not only in neurons but also in oligodendrocytes. We next examined the distribution of mGluR4 and 8 were expressed in excitatory or inhibitory neurons. Both mGluR4 and 8 were preferentially expressed in inhibitory neurons rather than in excitatory neurons. Futhermore, intrathecal delivery of CPPG, an antagonist for mGluR 4 and 8, attenuated nocifensive behaviors and the increase in fos positive-excitatory neurons of the dorsal horn induced by intraplantar injection of formalin. These findings suggest that mGluR4 and 8, which are preferentially expressed in inhibitory neurons, may play roles in the modulation of pain transmission through mGluRs in the spinal dorsal horn.
Learn More >Calcitonin gene-related peptide receptor has been implicated in the pathogenesis of migraine. Rimegepant is an orally administered, small-molecule, calcitonin gene-related peptide receptor antagonist that may be effective in acute migraine treatment.
Learn More >Spicy-food intake has been shown to affect various human physiological systems and diseases. This study tested the analgesia effect caused by stimulation of a spicy sensation (spicy stimulation) and explored the effect of spicy-food consumption on human basal pain sensitivity. A total of 60 healthy undergraduates were included in the primary study. Placebo and sweet stimulation were used as reference interventions. Pressure and cold-pain thresholds were measured before and after taste stimulation. The frequency of spicy-food intake was also evaluated. An additional 100 subjects were recruited to validate the results. Compared to placebo stimulation, both pressure and cold-pain thresholds increased during spicy stimulation (P<0.05). The increased thresholds remained, even when the taste stimulation residue was nearly eliminated (P<0.05). The pressure (10.0[2.1]vs.12.7[3.0]kg/cm, P<0.001) and cold-pain (4.4[1.6]vs.6.2[2.7]seconds, P=0.003) thresholds in subjects who consume spicy food ≥ 3 days/week were significantly lower than in those who consume it < 3 days/week. In the validation population, the frequency of spicy-food intake was negatively associated with subjects' pressure (β=-0.218, P=0.013) and cold-pain (β=-0.205, P=0.035) thresholds. Spicy stimulation has an analgesia effect on adults that persists even after the taste stimulation stops. Conversely, a long-term spicy diet can reduce the human basal pain threshold. TRIAL REGISTRATION: The study protocol was approved by the Medical Ethics Committee of the Second Affiliated Hospital of Army Medical University, People's Liberation Army (identification No., 2017-023-01), and it was registered on the Chinese Clinical Trial Registry at www.chictr.org.cn (No. ChiCTR1800015053). PERSPECTIVE: This study directly examined the effects of stimulation of a spicy sensation on adult pain sensitivity and was the first to explore the relationship between long-term spicy-food intake and human pain sensitivity. The results provide evidence for future clinical pain intervention and individualized pain treatment.
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