Articles: chronic-pain.
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Psychological bulletin · Nov 2011
ReviewPain, nicotine, and smoking: research findings and mechanistic considerations.
Tobacco addiction and chronic pain represent 2 highly prevalent and comorbid conditions that engender substantial burdens upon individuals and systems. Interrelations between pain and smoking have been of clinical and empirical interest for decades, and research in this area has increased dramatically over the past 5 years. We conceptualize the interaction of pain and smoking as a prototypical example of the biopsychosocial model. ⋯ We observed modest evidence that smoking may be a risk factor in the multifactorial etiology of some chronically painful conditions and that pain may come to serve as a potent motivator of smoking. We also found that whereas animal studies yielded consistent support for direct pain-inhibitory effects of nicotine and tobacco, results from human studies were much less consistent. Future research in the emerging area of pain and smoking has the potential to inform theoretical and clinical applications with respect to tobacco smoking, chronic pain, and their comorbid presentation. (PsycINFO Database Record (c) 2011 APA, all rights reserved).
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Genetic factors play a role in the etiology of persistent pain conditions, putatively by modulating underlying processes such as nociceptive sensitivity, psychological well-being, inflammation, and autonomic response. However, to date, only a few genes have been associated with temporomandibular disorders (TMD). This study evaluated 358 genes involved in pain processes, comparing allelic frequencies between 166 cases with chronic TMD and 1,442 controls enrolled in the OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment) study cooperative agreement. To enhance statistical power, 182 TMD cases and 170 controls from a similar study were included in the analysis. Genotyping was performed using the Pain Research Panel, an Affymetrix gene chip representing 3,295 single nucleotide polymorphisms, including ancestry-informative markers that were used to adjust for population stratification. Adjusted associations between genetic markers and TMD case status were evaluated using logistic regression. The OPPERA findings provided evidence supporting previously reported associations between TMD and 2 genes: HTR2A and COMT. Other genes were revealed as potential new genetic risk factors for TMD, including NR3C1, CAMK4, CHRM2, IFRD1, and GRK5. While these findings need to be replicated in independent cohorts, the genes potentially represent important markers of risk for TMD, and they identify potential targets for therapeutic intervention. ⋯ Genetic risk factors for TMD pain were explored in the case-control component of the OPPERA cooperative agreement, a large population-based prospective cohort study. Over 350 candidate pain genes were assessed using a candidate gene panel, with several genes displaying preliminary evidence for association with TMD status.
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Expert Rev Clin Pharmacol · Nov 2011
ReviewPharmacokinetic-pharmacodynamic modeling in acute and chronic pain: an overview of the recent literature.
In acute and chronic pain, the objective of pharmacokinetic-pharmacodynamic (PKPD) modeling is the development and application of mathematical models to describe and/or predict the time course of the pharmacokinetics (PK) and pharmacodynamics (PD) of analgesic agents and link PK to PD. Performing population PKPD modeling using nonlinear mixed effects modeling allows, apart from the estimation of fixed effects (the PK and PD model estimates), the quantification of random effects as within- and between-subject variability. Effect-compartment models and mechanism-based biophase distribution models that incorporate drug-association and -dissociation kinetics are applied in PKPD modeling of pain treatment. ⋯ Mixture models do not necessarily need to take PK data into account and allow the objective differentiation of measured responses to analgesics into specific response subgroups, and as such, may play an important role in analyzing Phase I and II analgesia studies. Appropriate application of PKPD modeling leads to the improvement of current therapeutics with respect to dose design and outcome, understanding the interaction of analgesics within complex chronic pain disease processes and may play an important role in drug development. In the current article, novel observations using the aforementioned techniques on opioids, NSAIDs, epidural analgesia, ketamine and GABA-ergic drugs in acute and chronic pain are discussed.
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Fibromyalgia (FM) is a chronic musculoskeletal pain syndrome which is characterised by clinical pain as well as widespread hyperalgesia/allodynia to mechanical, thermal, electrical, and chemical stimuli. Lack of consistent tissue abnormalities in FM patients has more and more shifted the focus away from peripheral factors and towards central nervous system abnormalities including central sensitisation as well as aberrant pain facilitation and inhibition. Besides quantitative sensory testing, functional brain imaging has been increasingly utilised to characterise the abnormal pain processing of FM patients. ⋯ Additionally, magnetic resonance spectroscopy studies demonstrated high concentration of the excitatory neurotransmitter glutamate in FM patients in pain-related brain areas which correlated not only with experimental but also with clinical pain ratings. Overall, functional brain imaging studies have provided compelling evidence for abnormal pain processing in FM, including brain activity that correlated with patients' augmented pain sensitivity (hyperalgesia/allodynia), temporal summation of pain, and prolonged pain aftersensations. Future imaging work needs to focus on identifying the neural correlates of FM patients' abnormal endogenous pain modulation which will likely not only shed more light on this important pain regulatory mechanism but may also provide useful information for future treatments of FM symptoms.
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Int J Clin Pharm Th · Nov 2011
Randomized Controlled TrialEfficacy and tolerability of flupirtine in subacute/ chronic musculoskeletal pain - results of a patient level, pooled re-analysis of randomized, double-blind, controlled trials.
Flupirtine, a nonopioid analgesic without antipyretic or antiphlogistic properties, constitutes a unique class within the group of WHO-I analgesics. First approved in Germany on a national level in 1989, this selective neuronal potassium channel opener evolved rapidly into one of the most preferred analgesics for the treatment of musculoskeletal pain in some European countries. However, its use outside Europe was limited due to a discrepancy between the empirical application of the drug and supporting evidence. As a consequence, the German Pain Society commissioned an independent research institute to perform a pooled re-analysis of all available data from randomized controlled trials (including some trial not yet published). ⋯ On the basis of this pooled analysis of individual data from 8 controlled clinical trials involving patients suffering from sub-acute/chronic musculoskeletal pain, the efficacy of flupirtine was superior to placebo across its effective and approved dosage range. Flupirtine was at least as active as the active comparators and showed a superior tolerability profile with a significantly lower treatment discontinuation rate.