The journal of pain : official journal of the American Pain Society
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The Communal Coping Model of Pain Catastrophizing in Daily Life: A Within-Couples Daily Diary Study.
The Communal Coping Model characterizes pain catastrophizing as a coping tactic whereby pain expression elicits assistance and empathic responses from others. Married couples (N = 105 couples; 1 spouse with chronic low back pain) completed electronic daily diary assessments 5 times/day for 14 days. In these diaries, patients reported pain catastrophizing, pain, and function, and perceived spouse support, perceived criticism, and perceived hostility. Non-patient spouses reported on their support, criticism, and hostility directed toward patients, as well as their observations of patient pain and pain behaviors. Hierarchical linear modeling tested concurrent and lagged (3 hours later) relationships. Principal findings included the following: a) within-person increases in pain catastrophizing were positively associated with spouse reports of patient pain behavior in concurrent and lagged analyses; b) within-person increases in pain catastrophizing were positively associated with patient perceptions of spouse support, criticism, and hostility in concurrent analyses; c) within-person increases in pain catastrophizing were negatively associated with spouse reports of criticism and hostility in lagged analyses. Spouses reported patient behaviors that were tied to elevated pain catastrophizing, and spouses changed their behavior during and after elevated pain catastrophizing episodes. Pain catastrophizing may affect the interpersonal environment of patients and spouses in ways consistent with the Communal Coping Model. ⋯ Pain catastrophizing may represent a coping response by which individuals' pain expression leads to assistance or empathic responses from others. Results of the present study support this Communal Coping Model, which emphasizes interpersonal processes by which pain catastrophizing, pain, pain behavior, and responses of significant others are intertwined.
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The objectives of this study were to demonstrate that empathy and validation could be increased in an observing partner who received a brief perspective-taking manipulation, resulting in less pain severity and greater pain tolerance in their partner, who experienced experimental pain. In addition, we examined the correlations between perceived empathy/validation and behavioral ratings of validation and invalidation. In 126 pain-free romantic couples, 1 partner was randomly assigned to complete the cold pressor task while the other observed. The couples were randomly assigned to a) a perspective-taking group in which observing partners were privately instructed to take the perspective of the pain participant; or b) a control group in which observing partners received only a description of the task. Compared with the control group, pain participants in the perspective-taking group reported that observing partners had been more validating during the task and they also reported significantly lower pain severity. In addition, pain participants' reports of their partners' validation and observing partners' self-reported empathic feelings were significantly related to lower pain severity over time. The results provide support that perspective taking may induce empathic feelings, in addition to perceptions of validation, which in turn promotes emotion regulation during pain. ⋯ The experimental evidence in this study suggests that empathic feelings can be induced in significant others with simple instructions, and this manipulation leads to less pain in their partners undergoing a painful task. The results suggest that perspective taking, empathy, and validation should be further investigated as pain intervention targets.
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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.