The journal of pain : official journal of the American Pain Society
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This study examined the impact of evidence concerning the presence of 1) a biomedical basis for pain and 2) psychosocial influences on practitioner appraisals of patient pain experiences. Furthermore, the potential moderating role of patient pain behavior was examined. In an online study, 52 general practitioners and 46 physiotherapists viewed video sequences of 4 patients manifesting pain, with accompanying vignettes describing presence or absence of medical evidence and psychosocial influences. Participants estimated pain intensity, daily interference, sympathy felt, effectiveness of pain medication, self-efficacy, their likability, and suspicions of deception. Primary findings indicated lower perceived pain and daily interference, less sympathy, lower expectations of medication impact, and less self-efficacy when medical evidence was absent. The same results were found when psychosocial influences were present, but only when the patient displayed higher levels of pain behavior. Furthermore, absence of medical evidence was related to less positive evaluations of the patients and to higher beliefs in deception in both professions. The presence of psychosocial influences was related to less positive evaluations and higher beliefs in deception in both professions. In sum, a range of contextual factors influence health care practitioner responses to patient pain. Implications for caregiving behavior are discussed. ⋯ The present study indicates that in the absence of clear medical evidence and in the presence of psychosocial influences, patient pain might be taken less seriously by health care practitioners. These findings are important to further understand the difficulties that relate to the clinical encounter between pain patients and health care practitioners.
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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.
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Changes in an individual's state-for example, anxiety/chronic pain-can modify the perception of action capabilities and physical task requirements. In parallel, considerable literature supports altered motor performance during both acute and chronic pain. This study aimed to determine the effect of experimental pain on perception of action capabilities and performance of a dynamic motor task. Performance estimates and actual performance of maximal single-leg hops were recorded for both legs in 13 healthy participants before, during, and after an episode of acute pain induced by a single bolus injection of hypertonic saline into vastus lateralis of 1 leg, with the side counterbalanced among participants. Both estimation of performance and actual performance were smaller (P < .01) during pain than before and after pain. This decrease in estimation and performance during pain was apparent for hops using either leg, but it was greater (P < .01) for the painful leg (-10.8 ± 12.1 cm) than for the control leg (-5.5 ± 7.9 cm). Participants accurately estimated their performance in all conditions for both legs. The results provide evidence that healthy participants have the ability to update the action-scaled relationship between perception and ability during acute pain. ⋯ This study demonstrates that the relationship between perceived physical ability and actual performance is effectively updated during acute muscle pain. This match between perceived ability and performance could be relevant during clinical pain assessment, with the potential to be a biomarker of transition from acute to chronic pain state.
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Second messengers mediating the expression of neuroplasticity in a model of chronic pain in the rat.
Hyperalgesic priming is a model of the transition from acute to chronic pain, in which previous activation of cell surface receptors or direct activation of protein kinase C epsilon markedly prolongs mechanical hyperalgesia induced by pronociceptive cytokines. We recently demonstrated a role of peripheral protein translation, alpha-calmodulin-dependent protein kinase II (αCaMKII) activation, and the ryanodine receptor in the induction of hyperalgesic priming. In the present study, we tested if they also mediate the prolonged phase of prostaglandin E2-induced hyperalgesia. We found that inhibition of αCaMKII and local protein translation eliminates the prolonged phase of prostaglandin E2 hyperalgesia. Although priming induced by receptor agonists or direct activation of protein kinase C epsilon occurs in male but not female rats, activation of αCaMKII and the ryanodine receptor also produces priming in females. As in males, the prolonged phase of prostaglandin E2-induced hyperalgesia in female rats is also protein kinase C epsilon-, αCaMKII-, and protein translation-dependent. In addition, in both male and female primed rats, the prolonged prostaglandin E2-induced hyperalgesia was significantly attenuated by inhibition of MEK/ERK. On the basis of these data, we suggest that the mechanisms previously shown to be involved in the induction of the neuroplastic state of hyperalgesic priming also mediate the prolongation of hyperalgesia. ⋯ The data provided by this study suggest that direct intervention on specific targets may help to alleviate the expression of chronic hyperalgesic conditions.