Pain
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Common cancers, including cancers of the breast, lung, and prostate, frequently metastasize to multiple bones where they can cause significant and life-altering pain. Similar to cancer itself, the factors that drive bone cancer pain evolve and change with disease progression. Once cancer cells have metastasized to bone, both the cancer cells and their associated stromal cells generate pain by releasing algogenic substances including protons, bradykinin, endothelins, prostaglandins, proteases, and tyrosine kinase activators. ⋯ Tumor growth in bone can also generate a neuropathic pain by directly injuring nerve fibers as well as inducing an active and highly pathological sprouting of both sensory and sympathetic nerve fibers that normally innervate the bone. This structural reorganization of sensory and sympathetic nerve fibers in the bone, combined with the cellular and neurochemical reorganization that occurs in the spinal cord and brain, appears to contribute to the peripheral and central sensitization that is common in advanced bone cancer pain. These mechanistic insights have begun to lead to advances in both how we understand and treat bone cancer pain.
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Randomized Controlled Trial
Addictive behaviors related to opioid use for chronic pain: A population-based study.
The growing body of research showing increased opioid use in patients with chronic pain coupled with concerns regarding addiction encouraged the development of this population-based study. The goal of the study was to investigate the co-occurrence of indicators of addictive behaviors in patients with chronic non-cancer pain in long-term opioid treatment. The study combined data from the individual-based Danish Health Survey in 2010 and the official Danish health and socio-economic, individual-based registers. ⋯ At least 2 of the 6 addictive behaviors were observed in 22.6% of the long-term opioid users with chronic pain compared with 11.5% of the non-opioid users with chronic pain and 8.9% of the individuals without chronic pain. Thus, a strong association was demonstrated between long-term opioid use and the clustering of addictive behaviors. An intricate relationship between chronic pain, opioid use, and addictive behaviors was observed in this study, which deserves both clinical attention and further research.
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Scientific evidence support the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals. Evidence of altered brain excitability emerged from clinical and preclinical investigation of sensory auras, ictal and interictal hypersensitivity to visual, auditory and olfactory stimulation, and reduced activation of descending inhibitory pain pathways. ⋯ Also, structural and functional alterations include the presence of subcortical white mater lesions, thickening of cortical areas involved in processing sensory information, and cortical neuroplastic changes induced by cortical spreading depression. Here, we review recent anatomical data on the trigeminovascular pathway and its activation by cortical spreading depression, a novel understanding of the neural substrate of migraine-type photophobia, and modulation of the trigeminovascular pathway by the brainstem, hypothalamus and cortex.
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Patients with low back pain (LBP; N = 102), fibromyalgia (FM; N = 100), and headache (HA; N = 100) were asked to describe their pain in their own words, and the words and phrases they used were then classified into 7 global domains (eg, Pain Quality, Pain Magnitude) and as many specific subdomains as needed to capture all of the ideas expressed (eg, under Pain Quality, subdomains such as sharp, achy, and throbbing). Fifteen pain quality subdomains were identified as most common. Nine of these demonstrated significant between-group differences in frequency. ⋯ The findings are generally consistent with a study that used similar procedures in other patient samples to identify the most common words patients use to describe pain, supporting their generalizability. The findings also support the use of pain quality measures for discriminating between chronic pain conditions. Finally, the findings have important implications for evaluating and modifying pain quality measures as needed.
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In order to understand how nociceptive information is processed in the spinal dorsal horn we need to unravel the complex synaptic circuits involving interneurons, which constitute the vast majority of the neurons in laminae I-III. The main limitation has been the difficulty in defining functional populations among these cells. We have recently identified 4 non-overlapping classes of inhibitory interneuron, defined by expression of galanin, neuropeptide Y (NPY), neuronal nitric oxide synthase (nNOS) and parvalbumin, in the rat spinal cord. ⋯ Parvalbumin cells did not express either activity-dependent marker following any of these stimuli. These results suggest that interneurons belonging to the NPY, nNOS and galanin populations are involved in attenuating pain, and for NPY and nNOS cells this is likely to result from direct inhibition of nociceptive projection neurons. They also suggest that the nociceptive inputs to the nNOS cells differ from those to the galanin and NPY populations.