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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Current approaches to classification of chronic pain conditions suffer from the absence of a systematically implemented and evidence-based taxonomy. Moreover, existing diagnostic approaches typically fail to incorporate available knowledge regarding the biopsychosocial mechanisms contributing to pain conditions. To address these gaps, the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks (ACTTION) public-private partnership with the U.S. Food and Drug Administration and the American Pain Society (APS) have joined together to develop an evidence-based chronic pain classification system called the ACTTION-APS Pain Taxonomy. This paper describes the outcome of an ACTTION-APS consensus meeting, at which experts agreed on a structure for this new taxonomy of chronic pain conditions. Several major issues around which discussion revolved are presented and summarized, and the structure of the taxonomy is presented. ACTTION-APS Pain Taxonomy will include the following dimensions: 1) core diagnostic criteria; 2) common features; 3) common medical comorbidities; 4) neurobiological, psychosocial, and functional consequences; and 5) putative neurobiological and psychosocial mechanisms, risk factors, and protective factors. In coming months, expert working groups will apply this taxonomy to clusters of chronic pain conditions, thereby developing a set of diagnostic criteria that have been consistently and systematically implemented across nearly all common chronic pain conditions. It is anticipated that the availability of this evidence-based and mechanistic approach to pain classification will be of substantial benefit to chronic pain research and treatment. ⋯ The ACTTION-APS Pain Taxonomy is an evidence-based chronic pain classification system designed to classify chronic pain along the following dimensions: 1) core diagnostic criteria; 2) common features; 3) common medical comorbidities; 4) neurobiological, psychosocial, and functional consequences; and 5) putative neurobiological and psychosocial mechanisms, risk factors, and protective factors.
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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.
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Scientific models are like tools, and like any tool they can be evaluated according to how well they achieve the chosen goals of the task at hand. In the science of treatment development for chronic pain, we might say that a good model ought to achieve at least 3 goals: 1) integrate current knowledge, 2) organize research and treatment development activities, and 3) create progress. In the current review, we examine models underlying current cognitive behavioral approaches to chronic pain with respect to these criteria. A relatively new model is also presented as an option, and some of its features examined. This model is called the psychological flexibility model. This model fully integrates cognitive and behavioral principles and includes a process-oriented approach of treatment development. So far it appears capable of generating treatment applications that range widely with regard to conditions targeted and modes of delivery and that are increasingly supported by evidence. It has led to the generation of innovative experiential, relationship-based, and intensive treatment methods. The scientific strategy associated with this model seeks to find limitations in current models and to update them. It is assumed within this strategy that all current treatment approaches will one day appear lacking and will change. ⋯ This Focus Article addresses the place of theory and models in psychological research and treatment development in chronic pain. It is argued that such models are not merely an academic issue but are highly practical. One potential model, the psychological flexibility model, is examined in further detail.