The journal of pain : official journal of the American Pain Society
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Comparative Study
Latent Class Analysis of the Short and Long-Form of the Chronic Pain Acceptance Questionnaire- Further Examination of Patient Subgroups.
A substantial literature indicates that pain acceptance is a useful behavioral process in chronic pain rehabilitation. Pain acceptance consists of willingness to experience pain and to engage in important activities even in the presence of pain and is often measured using the Chronic Pain Acceptance Questionnaire (CPAQ). Previous traditional cluster analyses of the 20-item CPAQ identified 3 patient clusters that differed across measures of patient functioning in meaningful ways. The aims of this study were to replicate the previous study in a new sample, using the more robust method of latent class analysis (LCA), and to compare the cluster structure of the CPAQ and the shorter CPAQ-8. In total, 914 patients with chronic pain completed the CPAQ and a range of measures of psychological and physical function. Patient clusters identified via LCA were then used to compare patients across functional measures. Contrary to previous research, LCA demonstrated that a 4-cluster structure was superior to a 3-cluster structure. Consistent with previous research, cluster membership based on patterns of pain willingness and activity engagement was significantly associated with specific patterns of psychological and physical function, in line with theoretical predictions. These cluster structures were similar for both CPAQ-20 and CPAQ-8 items. These results provide further evidence of the relevance of chronic pain acceptance, and a more nuanced understanding of how the components of acceptance are related to function. ⋯ Pain acceptance is important in chronic pain. The findings of the present study, which included 914 individuals with chronic pain, provide support for 4 discrete groups of patients based on levels of acceptance (low, medium, and high), as well as a group with a high level of activity engagement and low willingness to have pain. These groups appear statistically robust and differed in predictable ways across measures of functioning.
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Generalized dysfunction of the nociceptive system has been hypothesized to be an important pathophysiologic process underlying temporomandibular disorder (TMD) pain. Studies have not identified sensitization to painful stimuli administered prospectively across consecutive days among participants with TMD with chronic pain. We attempted to isolate an empirically derived laboratory-based marker of sustained mechanical pain sensitization. We examined whether this index accounted for variance in prospective assessments of clinical TMD pain. Participants were women with a clinical diagnosis of chronic TMD (n = 30) and healthy female controls (n = 30). Pain thresholds were assessed using digital algometry 4 times at 12-hour intervals over 48 consecutive hours and clinical TMD pain via follow-up telephone assessments. Sustained mechanical pain sensitization, defined by statistically significant linear decrements in pressure pain thresholds across the consecutive testing sessions, discriminated chronic TMD and control participants. An index of sustained sensitization at the masseter accounted for unique variance in clinical TMD pain over the subsequent 3-month assessment period, even controlling for mean pain threshold and baseline pain severity. These preliminary findings highlight discriminant and predictive validity characteristics of a novel marker of protracted pain sensitization among women with chronic TMD pain. ⋯ A laboratory-based and empirically defined marker of sustained mechanical pain sensitization over the course of days with acceptable discriminant and predictive validity was identified. This marker may represent a clinically useful marker of chronic TMD pain in women.
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Chronic sleep disturbance-induced stress is known to increase basal pain sensitivity. However, most surgical patients frequently report short-term sleep disturbance/deprivation during the pre- and postoperation periods and have normal pain perception presurgery. Whether this short-term sleep disturbance affects postsurgical pain is elusive. Here, we report that pre- or postexposure to rapid eye movement sleep disturbance (REMSD) for 6 hours daily for 3 consecutive days did not alter basal responses to mechanical, heat, and cold stimuli, but did delay recovery in incision-induced reductions in paw withdrawal threshold to mechanical stimulation and paw withdrawal latencies to heat and cold stimuli on the ipsilateral side of male or female rats. This short-term REMSD led to stress shown by an increase in swim immobility time, a decrease in sucrose consumption, and an increase in the level of corticosterone in serum. Blocking this stress via intrathecal RU38486 or bilateral adrenalectomy abolished REMSD-caused delay in recovery of incision-induced reductions in behavioral responses to mechanical, heat, and cold stimuli. Moreover, this short-term REMSD produced significant reductions in the levels of mu opioid receptor and kappa opioid receptor, but not Kv1.2, in the ipsilateral L4/5 spinal cord and dorsal root ganglia on day 9 after incision (but not after sham surgery). ⋯ Our findings show that short-term sleep disturbance either pre- or postsurgery does not alter basal pain perception, but does exacerbate postsurgical pain hypersensitivity. The latter may be related to the reductions of mu and kappa opioid receptors in the spinal cord and dorsal root ganglia caused by REMSD plus incision. Prevention of short-term sleep disturbance may help recovery from postsurgical pain in patients.
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Interactions between exogenous and endogenous opioids are not commonly investigated as a basis for sexually dimorphic opioid analgesia. We investigated the influence of spinal endomorphin 2 (EM2), an endogenous mu-opioid receptor (MOR) ligand, on the spinal antinociception produced by intrathecally administered opioids. Activation of spinal MORs facilitated spinal EM2 release. This effect was sexually dimorphic, occurring in males but not in females. Although activational effects of testosterone were required for opioid facilitation of spinal EM2 release in males, the absence of this facilitation in females did not result from either insufficient levels of testosterone or mitigating effects of estrogens. Strikingly, in males, the contribution of spinal EM2 to the analgesia produced by intrathecally applied MOR agonists depended on their analgesic efficacy relative to that of EM2. Spinal EM2 released by the higher efficacy MOR agonist sufentanil diminished sufentanil's analgesic effect, whereas EM2 released by the lower efficacy morphine had the opposite effect on spinal morphine antinociception. Understanding antithetical contributions of endogenous EM2 to intrathecal opioid antinociception not only enlightens the selection of opioid medications for pain management but also helps to explain variable sex dependence of the antinociception produced by different opioids, facilitating the acceptance of sexually dimorphic antinociception as a basic tenet. ⋯ The male-specific MOR-coupled enhancement of spinal EM2 release implies a parallel ability to harness endogenous EM2 antinociception. The inferred diminished ability of females to utilize the spinal EM2 antinociceptive system could contribute to their greater frequency and severity of chronic pain syndromes.