Pain
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Referred sensation (RS) as a specific clinical phenomenon has been known for a long time, although the underlying mechanisms remain unclear. The aims of this study were to assess if (1) healthy individuals who experienced RS had a less active endogenous pain system when compared with those who did not; (2) activation of descending pain inhibition mechanisms can modulate RS parameters; and finally, (3) a transient decrease in peripheral afferent input because of a local anesthetic (LA) block in the masseter muscle can modulate RS parameters. To assess these, 50 healthy participants were assessed in 3 different sessions. ⋯ In the second and third sessions, participants had their mechanical sensitivity and RS assessed before and after receiving an injection of 2 mL of LA and isotonic saline into the masseter muscle. The main findings of this study were (1) participants who experienced RS during standardized palpation exhibited increased mechanical sensitivity ( P < 0.05, Tukey post hoc test) and decreased CPM ( P < 0.05, Tukey post hoc test) when compared with those who did not; RS incidence ( P < 0.05, Cochran Q test), frequency ( P < 0.05; Friedman test), intensity ( P < 0.05, Tukey post hoc test), and area ( P < 0.05, Tukey post hoc test) were all significantly reduced when assessed (2) during a painful conditioning stimulus and (3) after LA block. These novel findings highlight that RS in the orofacial region are strongly modified by both peripheral and central nervous system factors.
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Dorsal root ganglia (DRG) neurons have been well described for their role in driving both acute and chronic pain. Although nerve injury is known to cause transcriptional dysregulation, how this differs across neuronal subtypes and the impact of sex is unclear. Here, we study the deep transcriptional profiles of multiple murine DRG populations in early and late pain states while considering sex. ⋯ We see both stereotyped and unique subtype signatures in injured states after nerve injury at both an early and late timepoint. Although all populations contribute to a general injury signature, subtype enrichment changes can also be seen. Within populations, there is not a strong intersection of sex and injury, but previously unknown sex differences in naïve states-particularly in Aβ-RA + Aδ-low threshold mechanoreceptors-still contribute to differences in injured neurons.
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Juvenile fibromyalgia (JFM) is a chronic widespread pain condition that primarily affects adolescent girls. Previous studies have found increased sensitivity to noxious pressure in adolescents with JFM. However, the underlying changes in brain systems remain unclear. ⋯ The JFM group showed augmented right primary somatosensory cortex (S1) activation to 4 kg/cm 2 (Z > 3.1, cluster-corrected P < 0.05), and the peak S1 activation magnitudes significantly correlated with the scores on the Widespread Pain Index ( r = 0.35, P = 0.048) with higher activation associated with more widespread pain. We also found that greater primary sensorimotor cortex activation in response to 4 kg/cm 2 mediated the between-group differences in pain intensity ratings ( P < 0.001). In conclusion, we found heightened sensitivity to noxious pressure stimuli and augmented pain-evoked sensorimotor cortex responses in adolescent girls with JFM, which could reflect central sensitization or amplified nociceptive input.
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Observational Study
Evidence of neuroinflammation in fibromyalgia syndrome: a [18F]DPA-714 positron emission tomography study.
This observational study aimed to determine whether individuals with fibromyalgia (FM) exhibit higher levels of neuroinflammation than healthy controls (HCs), as measured with positron emission tomography using [ 18 F]DPA-714, a second-generation radioligand for the translocator protein (TSPO). Fifteen women with FM and 10 HCs underwent neuroimaging. Distribution volume (V T ) was calculated for in 28 regions of interest (ROIs) using Logan graphical analysis and compared between groups using multiple linear regressions. ⋯ In support of our hypothesis, we found increased radioligand binding (V T ) in the FM group compared with HCs in several brain regions regardless of participants' TSPO binding status. The ROIs overlapped with prior reports of increased TSPO binding in FM. Overall, increasing evidence supports the hypothesis that FM involves microglia-mediated neuroinflammation in the brain.
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Endometriosis-related pain has been predominantly medically managed, which has hindered understanding of psychological factors involved in these pain experiences. Models of chronic pain highlight the biased interpretation of ambiguous information as health threat related (interpretation bias) as an important process in the development and maintenance of chronic pain. Whether interpretation bias may also be similarly implicated in endometriosis-related pain is unclear. ⋯ Within the endometriosis sample, interpretation bias was significantly associated with increases in pain-related interference, however, interpretation bias was not associated with any other pain outcomes and did not moderate the relationship between pain severity and pain interference. This study is the first to evidence biased interpretation styles among individuals with endometriosis and to show this bias is associated with pain interference. Whether interpretation bias varies over time and whether this bias can be modified through scalable and accessible interventions to alleviate pain-related interference are avenues for future research.