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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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.
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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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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 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.