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Chronic low back pain (LBP) caused by intervertebral disc herniation was reported in the 2010 Global Burden of Disease study to be the main reason for years lived with disability. It causes significant personal, social, and economic burdens. Many of those who suffer from LBP find conventional medical treatments to be unsatisfactory for treating their pain, so they are increasingly resorting to complementary and alternative medicine (CAM) therapies. Given that the population is aging, there is an urgent need to characterize the combinations of complementary therapies that yield the best outcomes and treatments, even for prolonged periods. This observational study aimed to evaluate the effect of ultramicronized palmitoylethanolamide (umPEA) + CAM (daily functional rehabilitation + decontracting massage) therapies on chronic pain in patients suffering from multiple herniated discs in the lumbar spine.
Neuropathic pain presents a huge societal and individual burden. The limited efficacy of current analgesics, diagnostic markers and clinical trial outcome measures arises from an incomplete understanding of the underlying mechanisms. A large and growing body of evidence has established the important role of microglia in the onset and possible maintenance of neuropathic pain, and these cells may represent an important target for future therapy. Microglial research has further revealed their important role in structural remodelling of the nervous system. In this review, we aim to explore the evidence for microglia in sculpting nervous system structure and function, as well as their important role in neuropathic pain, and finally integrate these studies to synthesize a new model for microglia in somatosensory circuit remodelling, composed of six key and inter-related mechanisms. Summarizing the mechanisms through which microglia modulate nervous system structure and function helps to frame a better understanding of neuropathic pain, and provide a clear roadmap for future research.
Overdose from opioids causes nearly 50 000 deaths in the US each year. Adverse consequences from opioid use are particularly pronounced among low-income and publicly insured individuals. However, little is known about patterns of opioid prescribing among non-US-born individuals in the US.
Studies in rodents suggest that cutaneous beta-2 adrenoceptors (β2-ARs) mediate inflammation and pain after tissue injury and that inflammation and peripheral nerve injury trigger increases in neuronal β2-AR expression. Hence, the aim of this study was to investigate the expression of β2-ARs on keratinocytes and dermal nerves in patients with complex regional pain syndrome (CRPS).
Few migraine preventive agents have been assessed in a pediatric population. We evaluated the safety and efficacy of cinnarizine and sodium valproate for migraine prophylaxis in children and adolescents.
To evaluate whether intraganglionic calcitonin gene-related peptide induced differential migraine-like responses in male and female rats.
Postoperative pain and opioid use are major challenges in perioperative medicine. Pain perception and its response to opioid use are multi-faceted and include pharmacological, psychological, and genetic components. Precision medicine is a unique approach to individualized health care in which decisions in management are based on genetics, lifestyle, and environment of each person. Genetic variations can have an impact on the perception of pain and response to treatment. This can have an effect on pain management in both acute and chronic settings. Although there is currently not enough evidence for making recommendations about genetic testing to guide pain management in the acute care setting, there are some known polymorphisms that play a role in surgical pain and opioid-related postoperative adverse outcomes. In this review, we describe the potential use of pharmacogenomics (PGx) for improving perioperative pain management. We first review a number of genotypes that have shown correlations with pain and opioid use and then describe the importance of PGx-guided analgesic protocols and implementation of screening in a preoperative evaluation clinical setting.
Cluster headache is a severe primary headache with a similar prevalence to that of multiple sclerosis. Cluster headache is characterised by unilateral trigeminal distribution of pain, ipsilateral cranial autonomic features, and a tendency to circadian and circannual periodicity.
To determine the magnitude of the association between cardiovascular disease and chronic musculoskeletal pain.
The cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs) is crucial for the regulation of inflammatory orofacial pain. Substance P (SP) plays an important role by activating neurokinin (NK)-I receptors in this cross-talk. Activation of extracellular signal-regulated kinase (ERK) 1/2, protein kinase A (PKA) and protein kinase C (PKC) in neurons and SGCs of peripheral ganglions by peripheral inflammation is associated with inflammatory hypersensitivity. This study tested the hypothesis that SP evoked SP-NK-I receptor positive feedback via the Renin Angiotensin System/B-Protein Kinase A-Rapidly Accelerates Fibrosarcoma-MEK-Extracellular Signal-Regulated Kinase (RAS/PKA-RAF-MEK-ERK) pathway, which is involved in pain hypersensitivity.Inflammatory models were induced in vivo by injecting Complete Freund's adjuvant (CFA) into the whisker pad of rats. SP was administrated to SGCs in vitro for investigating whether SP regulates the expression of NK-I receptor in the SGC nucleus. The effects of RAS-RAF-MEK, PKA and PKC pathways in this process were measured by co-incubating SGCs with respective Raf, PKA, PKC, and MEK inhibitors in vitro and by pre-injecting these inhibitors into the TGin vivo. SP significantly upregulated NK-I receptor, p-ERK1/2, Ras, B-Raf, PKA, and PKC in SGCs under inflammatory conditions. In addition, L703,606 (NK-I receptor antagonist), U0126 (MEK inhibitor), Sorafenib (Raf inhibitor) and H892HCL (PKA inhibitor) but not Chelerythrine chloride (PKC inhibitor) significantly decreased NK-I mRNA and protein levels induced by SP. The allodynia-related behavior evoked by CFA was inhibited by pre-injection of L703,606, U0126, Sorafenib and H892HCL into the TG. Overall, SP upregulates NK-I receptor in TG SGCs via PKA/RAS-RAF-MEK-ERK pathway activation, contributing to a positive feedback of SP-NK-I receptor in inflammatory orofacial pain.