The journal of pain : official journal of the American Pain Society
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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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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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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 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.