Articles: chronic.
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High-impact chronic pain (HICP), defined as chronic pain with a significant impact on daily function, affects approximately 8% of the Western population. In Denmark, HICP still remains to be described at the population level. Some patients with HICP are referred to the Danish pain centres, where they are registered with a procedural code. We conducted a nationwide registry-based study of all Danish patients registered with a visit to a pain centre from January 2005 to March 2022, to explore time trends in the prescription of analgesics and sedatives in this HICP subpopulation. Furthermore, data on socioeconomics and hospital diagnoses are reported. ⋯ This nationwide study of 66,577 Danish patients with high-impact chronic pain reveals a significant decrease in filled opioid prescriptions over the past 15 years, with a simultaneous rise in gabapentinoid use before referral to pain centres. These findings suggest a shift in clinical practice towards alternative pain management strategies. The study underscores the need for continued research into the long-term effects of these changes and their impact on patient outcomes.
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Opioid analgesics are commonly used to treat acute and chronic pain following traumatic injury. Psychiatric comorbidity has been reported to be associated with increased pain and persistent opioid use. Our aims were to determine the extent of post-injury opioid use and assess whether pre-injury antidepressant, benzodiazepine, and z-hypnotic drug use is associated with increased post-injury opioid use. ⋯ This large registry-based study adds to the body of knowledge on opioid use beyond in-hospital care in patients having sustained traumatic injury, a field which is scarcely investigated and not yet fully understood. It suggests that both previous drug therapy and the nature of opioid treatment initiation may affect outcome. This will help guide clinicians in selecting the appropriate pain management in this patient group.
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Memory biases for pain-related information may contribute to the development and maintenance of chronic pain; however, evidence for when (and for whom) these biases occur is mixed. Therefore, we examined neural, stress, and psychological factors that could influence memory bias, focusing on memories that motivate disabling behaviors: pain perception, conditioned responses to threat-and-safety cues, and responses to aversive nonnoxious stimuli. Two studies were conducted with adolescents with and without chronic pain. ⋯ However, no memory bias was present for the emotional response to an aversive stimulus (US; loud scream) or for the recall of pain intensity. Functional connectivity of the amygdala and hippocampus with memory circuits related to the degree of memory bias, but the specific connections varied between the studies, and we observed no relationship between memory bias and brain morphology. Our findings highlight the value of considering the interaction between implicit and explicit memory systems, contributing to a more comprehensive understanding of emotional memory biases in the context of chronic pain.
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Neuropathic pain is pain due to a disease or lesion of the somatosensory system, and can be either spontaneous, evoked or both. Hyperpathia is a type of evoked pain defined by IASP as 'a painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold'. The literature is sparse, and definitions are unclear and inconsistent. ⋯ Hyperpathia is a syndrome of evoked pain. It is poorly defined and little is known about its clinical presentation. Since it is part of pain symptomatology it is important to have a clear definition and understand the pathophysiology behind. This study explored signs of hyperpathia in a heterogeneous group of patients with peripheral neuropathic pain. We used stimulus-response function and repetitive pinprick stimulation to group patients based on the IASP definition. More studies are needed to understand how symptoms and signs coincide.
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High molecular weight hyaluronan (HMWH) inhibits hyperalgesia induced by diverse pronociceptive inflammatory mediators and their second messengers, in rats of both sexes. However, the hyperalgesia induced by ligands at 3 pattern recognition receptors, lipopolysaccharide (a toll-like receptor 4 agonist), lipoteichoic acid (a toll-like receptor 2/6 agonist), and nigericin (a NOD-like receptor family, pyrin domain containing 3 activator), and oxaliplatin and paclitaxel chemotherapy-induced peripheral neuropathy are only attenuated in males. After gonadectomy or intrathecal administration of an antisense to G-protein-coupled estrogen receptor 30 (GPER) mRNA, HMWH produces antihyperalgesia in females. ⋯ In females, hyperalgesia induced by PKCε agonist, ψεRACK, in control but not in primed nociceptors, was inhibited by HMWH. Inhibitors of 2 GPER second messengers, extracellular-regulated kinase 1/2 and nonreceptor tyrosine kinase, also unmasked HMWH antihyperalgesia in females with oxaliplatin chemotherapy-induced peripheral neuropathy, a condition in which nociceptors are primed as well as sensitized. Our results support GPER-dependent sex dimorphism in HMWH-induced antihyperalgesia for pain induced by pattern recognition receptor agonists, and chronic inflammatory and neuropathic pain, mediated by changes in signaling downstream of PKCε in primed nociceptors.