The journal of pain : official journal of the American Pain Society
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Lumbopelvic pain is common in pregnancy but the sensitization factors underlying the condition are largely unknown. This study characterized the somatosensory profile of pregnant and nonpregnant women and the relationship between pain, hypersensitivity, and commonly used manual clinical tests. Thirty-nine pregnant and 22 nonpregnant women were included. Although lumbopelvic pain was not an inclusion criterion, the pregnant women were divided into low- and high-pain groups following data collection. The sensitivity to light brush, pin-prick, and pressure pain was assessed bilaterally at 3 sites in the lumbopelvic region, at the shoulder, and in the lower leg. Responses to the active straight leg raise test and pain provocation tests of the sacroiliac joint were recorded. Participants completed questionnaires addressing emotional and physical well-being and rated disability using the Pelvic Girdle Questionnaire. Compared with controls, the high-pain group rated the active straight leg raise test as more difficult (P < .05), and both pain groups had more positive pain provocation tests (P < .05). The pregnant groups demonstrated significantly lower pressure pain thresholds at most assessment sites compared with controls (P < .05), but self-reported disability and pain were not correlated with pressure pain thresholds within pregnant participants. The high-pain group reported worse emotional health and poorer sleep quality than controls (P < .05). ⋯ This article presents the somatosensory profile of a healthy pregnant cohort. The results indicate that pain sensitivity increases during pregnancy possibly owing to the physical changes the body undergoes during pregnancy but also owing to changes in emotional health. This should be accounted for in clinical management of pregnant women with lumbopelvic pain.
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Despite evidence of autonomic disturbances in chronic multisymptom illnesses such as temporomandibular disorder (TMD) and fibromyalgia, additional work is needed to characterize the role of parasympathetic reactivity in these disorders. Given the high levels of comorbidity with psychiatric disorders characterized by stronger parasympathetic decline than controls in safe contexts (leading to higher arousal), it was hypothesized that individuals with TMD and fibromyalgia would respond similarly. In this preliminary investigation, 43 women with TMD (n = 17), TMD + fibromyalgia (n = 11), or neither (controls; n = 15) completed a baseline assessment of respiratory sinus arrhythmia (a measure of parasympathetic activity) followed by ongoing parasympathetic assessment during a questionnaire period. As predicted, patients showed greater parasympathetic decline during psychosocial assessment, suggesting an autonomic stance that supports defensive rather than engagement behaviors. Individual differences in parasympathetic reduction during the questionnaire period were related to a variety of physical and psychosocial variables. Although this study has a number of key limitations, including a convenience sampling approach and small group sizes, if replicated in larger samples, the findings would have important implications for the treatment of patients with these disorders. ⋯ Compared to controls, individuals with TMD or TMD and fibromyalgia demonstrated greater parasympathetic decline during psychosocial assessment, and individual differences in parasympathetic decline predicted negative patient outcomes. Such parasympathetic decline may demonstrate a tendency to readily perceive danger in safe environments.
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This study investigated the effects of a threatening and a safe social context on learning pain-related fear, a key factor in the development and maintenance of chronic pain. We measured self-reported pain intensity, pain expectancy, pain-related fear (verbal ratings and eyeblink startle responses), and behavioral measures of avoidance (movement-onset latency and duration) using an established differential voluntary movement fear conditioning paradigm. Participants (N = 42) performed different movements with a joystick: during fear acquisition, movement in one direction (CS+) was followed by a painful stimulus (pain-US) whereas movement in another direction (CS-) was not. For participants in the threat group, an angry face was continuously presented in the background during the task, whereas in the safe group, a happy face was presented. During the extinction phase the pain-US was omitted. As compared to the safe social context, a threatening social context led to increased contextual fear and facilitated differentiation between CS+ and CS- movements regarding self-reported pain expectancy, fear of pain, eyeblink startle responses, and movement-onset latency. In contrast, self-reported pain intensity was not affected by social context. These data support the modulation of pain-related fear by social context. ⋯ A threatening social context leads to stronger acquisition of (pain-related) fear and simultaneous contextual fear but does not affect pain intensity ratings. This knowledge may aid in the prevention of chronic pain and anxiety disorders and shows that social context might modulate pain-related fear without immediately affecting pain intensity itself.
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Skin temperature changes due to vasomotor disturbances are important features of complex regional pain syndrome (CRPS). Because this phenomenon has only been studied under controlled conditions, information on daily circadian variability is lacking. Also, studies in chronic CRPS patients with abnormal posturing, in which coldness of the affected extremity is more common, do not exist. We examined the response to external heating as well as circadian temperature changes over several days in the affected legs of 14 chronic CRPS patients with abnormal posturing and 17 controls. Skin temperatures were recorded hourly for 14 days using wireless sensors. Although the patients' affected extremities were significantly colder before external heating, the vasodilatory response was similar in the 2 groups. Additionally, median skin temperature differences between both legs and their variability was larger in patients than in controls during the day, but not during the night. These findings indicate that the mechanisms underlying impaired skin circulation in CRPS during daytime are reversible under certain circumstances. The large variation in skin temperature differences during the day questions the validity of using a single measurement in the diagnosis of CRPS, and our results indicate that only temperature differences >1.0 °C should be considered to reflect vasomotor disturbances. ⋯ This article shows that chronic CRPS patients have a normal vasodilatory response to external heating and that skin temperature differences between the affected and unaffected lower limbs, which were highly variable during daytime, disappeared during sleep. This indicates that part of the vasomotor regulation in these patients is still functional.
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Chronic neuropathic pain is often difficult to treat with current pain medications. Gene therapy is presently being explored as a therapeutic approach for the treatment of neuropathic and cancer pain. In this study, we sought to use an injury-specific promoter to deliver the mu-opioid receptor (MOR) transgene such that expression would occur during the injured state only in response to release of injury-specific galanin. To determine whether an injury-specific promoter can produce neuron-specific MOR expression and enhanced antinociception, we compared animals infected with a galanin promoter virus (galMOR) or a human cytomegalovirus promoter virus (cmvMOR). In behavioral assays, we found an earlier onset and a larger magnitude of antinociception in animals infected with galMOR compared with cmvMOR. Immunohistochemical analysis of dorsal root ganglion neurons revealed a significant increase in MOR-positive staining in cmvMOR- and galMOR-treated mice. Spinal cord sections from galMOR-treated mice showed a greater increase in density but not area of MOR-positive staining. These results suggest that using injury-specific promoters to drive gene expression in primary afferent neurons can influence the onset and magnitude of antinociception in a rodent model of neuropathic pain and can be used to upregulate MOR expression in populations of neurons that are potentially injury specific. ⋯ An injury-specific promoter (galMOR) was used to drive MOR expression in a population- and injury-specific manner. GalMOR increased antinociception and density of MOR staining in the spinal cord. This article presents evidence that promoter selection is an important component in successful gene expression in an injury- and population-specific manner.