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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The anterior cingulate cortex (ACC) modulates emotional responses to pain. Whereas, the caudal ACC (cACC) promotes expression of pain affect, the rostral ACC (rACC) contributes to its suppression. Both subdivisions receive glutamatergic innervation, and the present study evaluated the contribution of N-methyl-d-aspartic acid (NMDA) receptors within these subdivisions to rats' expression of pain affect. ⋯ These findings demonstrate that NMDA receptor agonism within the cACC and rACC either increases or decreases emotional responses to noxious stimulation, respectively. PERSPECTIVE: NMDA receptor activation of the rostral and caudal ACC respectively inhibited or enhanced rats' emotional response to pain. These findings mirror those obtained from human neuroimaging studies; thereby, supporting the use of this model system in evaluating the contribution of ACC to pain affect.
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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.
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Chronic overlapping pain conditions (COPCs) are a set of painful chronic conditions characterized by high levels of co-occurrence. It has been hypothesized that COPCs co-occur in many cases because of common neurobiological vulnerabilities. In practice, most research on COPCs has focused upon a single index condition with little effort to assess comorbid painful conditions. ⋯ The codes presented can facilitate administrative database research on COPCs. PERSPECTIVE: This article presents a set of ICD-10 codes that researchers can use to explore the presence and overlap of COPCs in administrative databases. This may serve as a tool for estimating samples for research, exploring comorbidities, and treatments for individual COPCs, and identifying mechanisms associated with their overlap.