The journal of pain : official journal of the American Pain Society
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Multicenter Study Observational Study
Classification of and risk factors for estrogen deprivation pain syndromes related to aromatase inhibitor treatments in women with breast cancer: a prospective multicenter cohort study.
Aromatase inhibitors (AIs) are the first-line treatment in women with breast cancer for total estrogen depletion. Half the treated women may develop pain, and this condition may therefore be seen as a clinical model of pain related to estrogen deprivation. In this prospective multicenter study, we classified AI-related pain syndromes and identified their predictors. A 1-year, prospective, multicenter cohort study, with 6 visits, was carried out on 135 women with early-stage breast cancer and no pain at the start of AI treatment. At initial assessment, we investigated clinical (demographic and psychosocial, cancer characteristics and treatment, sleep, quality of life), biological (sex hormones, vitamin D, bone biomarkers, oxidative stress, immunologic and inflammatory markers), environmental, and genetic (polymorphism for pain mechanisms) risk factors for pain. During 1 year of follow-up, 77 women (57%) developed pain, leading to AI discontinuation in 12 cases. Five pain syndromes were identified: joint pain (36%), diffuse pain (22%), tendinitis (22%), neuropathic pain (9%), and mixed pain (11%), which are mostly persistent (57%), with diffuse and joint pains the most intense. Risk factors for the development of pain included higher levels of anxiety and impaired quality of life at the initial assessment, whereas cancer characteristics, genetic background, inflammation, and immunologic and hormonal status at baseline were not significant predictors. ⋯ This article presents a classification of AI-related pain syndromes induced by estrogen deprivation that were previously described as arthralgia, but not as neuropathic, diffuse, and mixed pain. This estrogen deprivation-related condition represents a clinical model of pain, and our study identified mostly psychological risk factors for pain development.
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Deep brain stimulation (DBS) of the periventricular/periaqueductal gray area and sensory thalamus can reduce pain intensity in patients with neuropathic pain. However, little is known about its impact on quality of life, emotional well-being, and cognition. This study followed up 18 patients who had received DBS for neuropathic pain. Each participant had previously undergone psychometric evaluation of each of the above areas as part of a routine presurgical neuropsychological assessment. Commensurate measures were employed at a follow-up assessment at least 6 months postsurgery. DBS significantly improved mood, anxiety, and aspects of quality of life. Improvements correlated with reduced pain severity. However, the sample continued to show impairments in most areas when compared against normative data published on nonclinical samples. There was little change in general cognitive functioning, aside from deterioration in spatial working memory. However, improvements in pain severity were associated with less improvement (and even deterioration) on measures of executive cognitive functioning. Improvements in emotional well-being also were correlated with changes in cognition. These results suggest that DBS of the periventricular/periaqueductal gray and/or sensory thalamus improves quality of life and emotional well-being in sufferers, although there is some indication of executive dysfunction, particularly among those reporting greatest pain alleviation. ⋯ This article examines the neuropsychological outcomes of DBS surgery as a treatment for neuropathic pain. This intervention was found to improve pain severity, emotional well-being, and quality of life, although such benefits may be accompanied by reduced ability on tasks measuring executive functioning.
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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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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.