The journal of pain : official journal of the American Pain Society
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Observational Study
Attachment styles, pain, and the consumption of analgesics during labor: a prospective observational study.
Individuals with less secure attachment styles have been shown to experience more pain than people with more secure attachment styles; however, attachment styles have not yet been examined in the context of labor pain and analgesic consumption. The purpose of this prospective observational study was to assess the influence of the mother's attachment style on the perception of labor pain, as assessed by a visual analog scale and analgesic consumption. Eighty-one pregnant women with a mean age of 32 years (standard deviation = 5.1) were assessed during the third trimester of pregnancy and during labor. The physical predictors of labor pain were recorded, and the adult attachment style was assessed with the Adult Attachment Scale-Revised. For labor analgesia, a low dose of patient-controlled epidural analgesia protocol (ropivacaine .6 mg/mL plus sufentanil .5 μg/mL) was used. Women with a secure attachment style reported significantly less labor pain (P < .001) and a significantly lower analgesic consumption during labor (P < .001) than insecurely attached women. These findings suggest that women's attachment style was associated with labor pain and analgesic consumption and support the relevance of the attachment theory as a promising conceptual framework for understanding labor pain. ⋯ This study showed that women with an insecure attachment style were more likely to report higher pain before patient-controlled epidural analgesia and higher analgesic consumption and to request supplemental analgesia during labor. The assessment of adult attachment has the potential to identify women at high risk of poorly coping with pain during childbirth.
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This study tested the effects of aging and race on responses to noxious stimuli using a wide range of stimulus modalities. The participants were 53 non-Hispanic blacks and 138 non-Hispanic white adults, ages 45 to 76 years. The participants completed a single 3-hour sensory testing session where responses to thermal, mechanical, and cold stimuli were assessed. The results suggest that there are selected age differences, with the older group less sensitive to warm and painful heat stimuli than middle-aged participants, particularly at the knee. This site effect supports the hypothesis that the greatest decrement in pain sensitivity associated with aging occurs in the lower extremities. In addition, there were several instances where age and race effects were compounded, resulting in greater race differences in pain sensitivity among the older participants. Overall, the data suggest that previously reported race differences in pain sensitivity emerged in our older samples, and this study contributes new findings in that these differences may increase with age in non-Hispanic blacks for temporal summation and both heat and cold immersion tolerance. We have added to the aging and pain literature by reporting several small to moderate differences in responses to heat stimuli between middle- and older-age adults. ⋯ This study found that the greatest decline in pain sensitivity with aging occurs in the lower extremities. In addition, race differences in pain sensitivity observed in younger adults were also found in our older sample.
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This study examined the role of the glial-neuronal G protein-coupled receptor kinase 2 (GRK2) pathway in the development of trigeminal neuropathic pain. Male Sprague Dawley rats, weighing 220 to 240 g, were anesthetized with ketamine (0.2 g/kg) and xylazine (0.02 g/kg). Under anesthesia, the left lower second molar was extracted, followed by the placement of a mini-dental implant to intentionally injure the inferior alveolar nerve. This injury produced mechanical allodynia along with the downregulation of neuronal GRK2 expression in the medullary dorsal horn. On the other hand, early intracisternal treatment with MDL28170, a calpain inhibitor, produced prolonged antiallodynic effects and blocked this downregulation of neuronal GRK2 expression. The intracisternal infusion of minocycline, a microglia inhibitor, and l-α-aminoadipic acid, an astrocytic specific inhibitor, also blocked the induced mechanical allodynia and downregulated neuronal GRK2 expression, respectively. Double immunofluorescence showed that the interleukin (IL)-1β and IL-1R signals colocalize with the astrocytes and neurons, respectively, in the medullary dorsal horn following an inferior alveolar nerve injury. In addition, the intracisternal infusion of an IL-1 receptor antagonist also produced antiallodynic effects and blocked the downregulation of neuronal GRK2 expression. These results suggest that the glial-neuronal GRK2 pathway is a potentially important new target for treating neuropathic pain. Moreover, the IL-1β expressed in astrocytes plays a significant role in modulating this pathway. ⋯ This study showed that the glial-neuronal GRK2 pathway participates in the development of trigeminal neuropathic pain in rats. These results suggest that the glial-neuronal GRK2 pathway is a potentially important new target for the treatment of neuropathic pain.