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Effects from cognitive performance on pain tolerance have been documented, however, sample sizes are small and confounders often overlooked. We aimed to establish that performance on neuropsychological tests was associated with pain tolerance, controlling for salient confounders.
Learn More >Chronic low back pain due to lumbar spinal stenosis (LSS) is common, costly, mechanistically complex, and clinically challenging. However, the factors and mechanisms causing and mediating chronic pain induced by cauda equina compression remain unclear. Here, we examined the role of cyclooxygenase (COX)-2 in infiltrated macrophages, a key mediator of inflammation, in chronic neuropathic pain by LSS using an animal model. LSS was induced in adult male rats by cauda equina compression procedure using a silicone block within the epidural spaces of L5-L6 vertebrae. Locomotor deficit was observed after compression and mechanical allodynia was developed progressively for 4 weeks after injury. A number of macrophage were also infiltrated into the spinal parenchyma and cauda equina and COX-2 was expressed in infiltrated macrophages at 28 days after cauda equina compression. The administration of COX-2 inhibitors, celecoxib and MPO-0029, significantly alleviated LSS-induced chronic mechanical allodynia and inhibited the mRNA expression of inflammatory mediators such as tnf-α, Il-1β, il-6, and inos. Furthermore, COX-2 inhibitors significantly reduced prostaglandin E2 production. These results demonstrated the role of COX-2 in LSS-induced chronic neuropathic pain and suggest that the regulation of COX-2 can be considered as a therapeutic target to relive neuropathic pain.
Learn More >Diabetes mellitus is becoming increasingly common worldwide. As this occurs, there will be an increase in the prevalence of known comorbidities from this disorder of glucose metabolism. One of the most disabling adverse comorbidities is diabetic neuropathy. The most common neuropathic manifestation is distal symmetric polyneuropathy, which can lead to sensory disturbances, including diminished protective sense, making patients prone to foot injuries. However, focal, multifocal, and autonomic neuropathies are also common. Diabetic nerve pain and Charcot osteoarthropathy are advanced neuropathic conditions that portend a severe deterioration in quality of life. To combat these symptoms, along with glycemic control and establishment of health care systems to educate and support patients with the complexities of diabetes, there are pharmacologic remedies to ameliorate the neurologic symptoms. Several guidelines and review boards generally recommend the use of tricyclic antidepressants, serotonin/norepinephrine-reuptake inhibitors, α-2-delta ligands, and anticonvulsants as medications to improve painful diabetic neuropathy and quality of life.
Learn More >1) To assess the feasibility of research methods to test a self-management intervention aimed at preventing acute to chronic pain transition in patients with major lower extremity trauma (iPACT-E-Trauma) and 2) to evaluate its potential effects at three and six months postinjury. Design. A pilot randomized controlled trial (RCT) with two parallel groups.
Learn More >Central pain associated with changes in sensory thresholds is one of the most enduring consequences of major trauma. Yet it remains sparsely studied among community-dwelling survivors of moderate-to-severe traumatic brain injury (TBI).
Learn More >This study quantified risks of cardiovascular, cerebrovascular, and mortality events among patients with migraine receiving prophylaxis.
Learn More >The diverse etiologies of conditions characterized by chronic pain require molecular assessment. Over recent decades, progress in research has enabled studying of the genetic mechanisms underlying pain and consequently realistic clinical solutions. Genetic linkage has unveiled rare single-gene contributions to pain disorders, whilst advances in genome-wide association studies (GWAS) define multigenic mechanisms in conditions such as back pain and migraine. Advances in DNA sequencing now additionally allow us to efficiently identify mutations underlying congenic pain syndromes and diagnose individuals at risk of developing ongoing pain. In the laboratory, targeted modulation of gene expression with RNA interference, as well as the development of transgenic mouse models, has exponentially expanded our ability to interrogate the molecular cascades behind nociceptive and chronic pain. Furthermore, the recent evolution of CRISPR/Cas9 mediated gene editing has produced a simple yet effective method of altering the genome to alleviate ongoing pain. This genetic revolution will undoubtedly lead to more personalized therapeutics, which with consideration of environmental risk factors should combat clinical pain. We believe these improvements will occur in the next few decades. A video accompanying this abstract is available online as Supplemental Digital Content at http://links.lww.com/PAIN/A804.
Learn More >Multiple cranial nerve blocks of the greater and lesser occipital, supraorbital, supratrochlear and auriculotemporal nerves are widely used in the treatment of primary headaches. We present efficacy and safety data for these procedures.
Learn More >The impact of vitamin D on sensory function, including pain processing, has been receiving increasing attention. Indeed, vitamin D deficiency is associated with various chronic pain conditions, and several lines of evidence indicate that vitamin D supplementation may trigger pain relief. However, the underlying mechanisms of action remain poorly understood. We used inflammatory and non-inflammatory rat models of chronic pain to evaluate the benefits of vitamin D (cholecalciferol) on pain symptoms. We found that cholecalciferol supplementation improved mechanical nociceptive thresholds in monoarthritic animals and reduced mechanical hyperalgesia and cold allodynia in a model of mononeuropathy. Transcriptomic analysis of cerebrum, dorsal root ganglia, and spinal cord tissues indicate that cholecalciferol supplementation induces a massive gene dysregulation which, in the cerebrum, is associated with opioid signaling (23 genes), nociception (14), and allodynia (8), and, in the dorsal root ganglia, with axonal guidance (37 genes) and nociception (17). Among the identified cerebral dysregulated nociception-, allodynia-, and opioid-associated genes, 21 can be associated with vitamin D metabolism. However, it appears that their expression is modulated by intermediate regulators such as diverse protein kinases and not, as expected, by the vitamin D receptor. Overall, several genes-Oxt, Pdyn, Penk, Pomc, Pth, Tac1, and Tgfb1-encoding for peptides/hormones stand out as top candidates to explain the therapeutic benefit of vitamin D supplementation. Further studies are now warranted to detail the precise mechanisms of action but also the most favorable doses and time windows for pain relief.
Learn More >The current Phase 2b study aimed to evaluate the efficacy of mindfulness-based cognitive therapy for migraine (MBCT-M) to reduce migraine-related disability in people with migraine.
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