The journal of pain : official journal of the American Pain Society
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Randomized Controlled Trial Comparative Study
Moderators of mindfulness meditation, cognitive therapy, and mindfulness-based cognitive therapy for chronic low back pain: A test of the Limit, Activate and Enhance model.
This study examined psychosocial pain treatment moderation in a secondary analysis of a trial that compared cognitive therapy (CT), mindfulness-meditation (MM), and mindfulness-based cognitive therapy (MBCT) for chronic low back pain (CLBP). The Limit, Activate, and Enhance (LA&E) model of moderation provided a framework for testing a priori hypotheses. Adult participants (N = 69) with CLBP completed a pretreatment assessment of hypothesized moderators: pain catastrophizing, brain state as assessed by electroencephalogram, mindful observing, and nonreactivity. ⋯ Theory-driven moderation research has the capacity to inform the development of patient-treatment matching algorithms to optimize outcome. PERSPECTIVE: This study presents preliminary findings from theory-driven tests of the moderators of mindfulness meditation, cognitive therapy, and mindfulness-based cognitive therapy for chronic low back pain. The results of such analyses may inform the understanding of for whom various evidence-based psychosocial pain treatments may engender the most meaningful benefits.
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Research in adult populations indicates that several sociodemographic and environmental variables increase risk for pain and poor outcomes. There is little research exploring the impact of household income, health insurance coverage, barriers to health care, neighborhood and school safety, violence experienced, and neighborhood isolation on pediatric chronic pain. Data from the Add Health Study, a longitudinal examination of a nationally-representative adolescent sample were analyzed. ⋯ PERSPECTIVE: Adolescents with chronic pain had lower income, and more health care barriers, safety concerns, and violence exposure compared to those without chronic pain. Access to care is a significant problem in youth with chronic pain. The relationships between race/ethnicity, risk factors, and health outcomes are complex and require additional research.
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Research into potentially novel biomarkers for chronic pain development is lacking. microRNAs (miRNAs) are attractive candidates as biomarkers due to their conservation across species, stability in liquid biopsies, and variation that corresponds to a pathologic state. miRNAs can be sorted into extracellular vesicles (EVs) within the cell and released from the site of injury. EVs transfer cargo molecules between cells thus affecting key intercellular signaling pathways. The focus of this study was to determine the plasma derived EV miRNA content in a chronic neuropathic pain rat model. ⋯ PERSPECTIVE: This article describes the DE miRNA content of plasma derived EVs, comparing neuropathic pain to normal conditions. This data indicates that EV miRNAs may be important in nociception and may also serve as biomarkers for chronic pain. These results encourage further research on EV miRNAs in chronic neuropathic pain sufferers.
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Vincristine, oxaliplatin, and cisplatin are commonly prescribed chemotherapeutic agents for the treatment of many tumors. However, a main side effect is chemotherapy-induced peripheral neuropathy (CIPN), which may lead to changes in chemotherapeutic treatment. Although symptoms associated with CIPN are recapitulated by mouse models, there is limited knowledge of how these drugs affect the expression of genes in sensory neurons. ⋯ Treatment with cisplatin resulted in a mixed gene expression signature. PERSPECTIVE: These results provide insight into the recruitment of immune responses to dorsal root ganglia and indicate enhanced neuroinflammatory processes following administration of vincristine, oxaliplatin, and cisplatin. These gene expression signatures may provide insight into novel drug targets for treatment of CIPN.
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Orofacial pain is characterized by its easy spread to adjacent areas, thus presenting with primary hyperalgesia (hypersensitivity at the site of injury) and secondary hyperalgesia (extraterritorial hypersensitivity outside the injured zone). However, the mechanisms behind the secondary hyperalgesia are poorly understood. In the present study, we used a mouse model of partial transection of the infraorbital nerve (pT-ION) to study whether calcium channel subunit α2δ1 (Cavα2δ1) and its downstream signaling contributes to the development of secondary hyperalgesia in the orofacial area. pT-ION caused primary (V2 skin) and secondary (V3 skin) hyperalgesia, which was reversed by the Cavα2δ1 antagonist gabapentin and by the expression of Cavα2δ1-targeting interfering RNA in trigeminal ganglion (TG)-V3 neurons. pT-ION induced increased expression of PKC and TRPA1, which was reversed by Cavα2δ1-targeting interfering RNA, and PKC inhibition reversed the upregulation of TRPA1 and gap junction (GJ) proteins induced by pT-ION. ⋯ Thus, we conclude that Cavα2δ1 contributes to the development of secondary hyperalgesia through its downstream PKC-TRPA1/GJ signaling pathways. PERSPECTIVE: This study demonstrates that the activation of Cavα2δ1 and the downstream PKC-TRPA1/GJ signaling pathway contributes greatly to trigeminal nerve injury-induced secondary mechanical and cold hyperalgesia. This suggests that inhibitors of Cavα2δ1, TRPA1, or GJs might be effective treatments for nerve injury-induced spreading of orofacial pain.