Kynurenine Pathway Metabolites as Potential Biomarkers in Chronic Pain.

Chronic pain is a pressing medical and socioeconomic issue worldwide. It is debilitating for individual patients and places a major burden on society in the forms of direct medical costs and lost work productivity. Various biochemical pathways have been explored to explain the pathophysiology of chronic pain in order to identify biomarkers that can potentially serve as both evaluators of and guides for therapeutic effectiveness. The kynurenine pathway has recently been a source of interest due to its suspected role in the development and sustainment of chronic pain conditions. The kynurenine pathway is the primary pathway responsible for the metabolization of tryptophan and generates nicotinamide adenine dinucleotide (NAD+), in addition to the metabolites kynurenine (KYN), kynurenic acid (KA), and quinolinic acid (QA). Dysregulation of this pathway and changes in the ratios of these metabolites have been associated with numerous neurotoxic and inflammatory states, many of which present simultaneously with chronic pain symptoms. While further studies utilizing biomarkers to elucidate the kynurenine pathway's role in chronic pain are needed, the metabolites and receptors involved in its processes nevertheless present researchers with promising sources of novel and personalized disease-modifying treatments.

Identifying molecular mechanisms of acute to chronic pain transition and potential drug targets.

INTRODUCTION: Chronic pain is pain that lasts more than the normal physiologic healing time at the time of initial insult. The transition from acute to chronic pain has been studied thoroughly. Understanding the mechanisms underlying chronic pain formation is essential for the development of novel treatments and therapeutics for chronic pain prevention. AREA COVERED: The transition from acute to chronic pain has been associated with the intracellular changes caused by repeated stimulus application, or neuronal priming, allowing for the chronicity of pain. Ongoing research studies have shown this priming to occur at various sites along the pathway for the neural transmission of pain. The purpose of this review is to not only elucidate the transition from acute to chronic pain and discuss current studies/trials related to this transition but also to highlight mechanisms involved in the process that could serve as potential targets for chronic pain prevention. EXPERT OPINION: We are providing an overview of novel treatment strategies for preventing the transition from acute to chronic pain. A multifaceted and multimodal approach that invokes multiple targets, at least one from each section (the periphery, the spinal cord, and the brain), would be the best option for tackling this problem.

Dehiscence and Deep Wound Infection After Spinal Cord Stimulator Implant Managed Without Explantation: A Case Report.

Deep infections of spinal cord stimulator devices usually result in explantation, as recommended by some professional societies. However, alternative options should be explored to avoid potential complications that are associated with explantation, and possibly additional procedures required in consideration of reimplantation. In this case, the patient presented with wound dehiscence after implantation. There was suspicion for deep wound infection based on a wound culture that was positive for Staphylococcus aureus, but no purulent material was noted on further inspection. The patient was treated with standard wound-care management and oral antibiotics without removing the device, and recovered while preserving the original system.