YokoCo

To analyze the clinical manifestations and imaging features of a hospitalized patient with intermittent headache who was finally diagnosed with von Hippel-Lindau (VHL) syndrome and to perform whole-exon gene detection to improve the understanding of the diagnosis and treatment strategies of the disease.

Percutaneous balloon compression (PBC) is an effective and well-established surgery for treating trigeminal neuralgia (TN). However, if the initial attempt fails to produce a distinct pear shape, there is no conventional strategy to follow: repeat a few days later or re-puncture?

Osteoarthritis (OA) reduces the quality of life as a result of the pain caused by continuous joint destruction. Inactivated (LA-1) ameliorated osteoarthritis and protected cartilage by modulating inflammation. In this study, we evaluated the mechanism by which live LA-1 ameliorated OA. To investigate the effect of live LA-1 on OA progression, we administered LA-1 into monosodium iodoacetate (MIA)-induced OA animals. The pain threshold, cartilage damage, and inflammation of the joint synovial membrane were improved by live LA-1. Furthermore, the analysis of intestinal tissues and feces in the disease model has been shown to affect the systems of the intestinal system and improve the microbiome environment. Interestingly, inflammation of the intestinal tissue was reduced, and the intestinal microbiome was altered by live LA-1. Live LA-1 administration led to an increase in the level of which is a short-chain fatty acid (SCFA) butyrate-producing bacteria. The daily supply of butyrate, a bacterial SCFA, showed a tendency to decrease necroptosis, a type of abnormal cell death, by inducing autophagy and reversing impaired autophagy by the inflammatory environment. These results suggest that OA is modulated by changes in the gut microbiome, suggesting that activation of autophagy can reduce aberrant cell death. In summary, live LA-1 or butyrate ameliorates OA progression by modulating the gut environment and autophagic flux. Our findings suggest the regulation of the gut microenvironment as a therapeutic target for OA.

Temporomandibular disorders (TMD) involve chronic pain in the masticatory muscles and jaw joints, but the mechanisms underlying the pain are heterogenous and vary across individuals. In some cases, structural, functional, and metabolic changes in the brain may underlie the condition. In the present study, we evaluated the functional connectivity between 86 regions of interest (ROIs), which were chosen based on previously reported neuroimaging studies of pain and differences in brain morphology identified in an initial surface-based morphometry analysis. Our main objectives were to investigate the topology of the network formed by these ROIs and how it differs between individuals with TMD and chronic pain ( = 16) and pain-free control participants ( = 12). In addition to a true resting state functional connectivity scan, we also measured functional connectivity during a 6-min application of a noxious cuff stimulus applied to the left leg. Our principal finding is individuals with TMD exhibit more suprathreshold correlations (higher nodal degree) among all ROIs but fewer "hub" nodes (i.e., decreased betweenness centrality) across conditions and across all pain pathways. These results suggest is this pain-related network of nodes may be "over-wired" in individuals with TMD and chronic pain compared to controls, both at rest and during experimental pain.

Rheumatic diseases, such as osteoarthritis and rheumatoid arthritis, affect over 750 million people worldwide and contribute to approximately 40% of chronic pain cases. Inflammation and tissue damage contribute to pain in rheumatic diseases, but pain often persists even when inflammation/damage is resolved. Mechanisms that cause this persistent pain are still unclear. Mitochondria are essential for a myriad of cellular processes and regulate neuronal functions. Mitochondrial dysfunction has been implicated in multiple neurological disorders, but its role in sensory processing and pain in rheumatic diseases is relatively unexplored. This review provides a comprehensive understanding of how mitochondrial dysfunction connects inflammation and damage-associated pathways to neuronal sensitization and persistent pain. To provide an overall framework on how mitochondria control pain, we explored recent evidence in inflammatory and neuropathic pain conditions. Mitochondria have intrinsic quality control mechanisms to prevent functional deficits and cellular damage. We will discuss the link between neuronal activity, mitochondrial dysfunction and chronic pain. Lastly, pharmacological strategies aimed at reestablishing mitochondrial functions or boosting mitochondrial dynamics as therapeutic interventions for chronic pain are discussed. The evidence presented in this review shows that mitochondria dysfunction may play a role in rheumatic pain. The dysfunction is not restricted to neuronal cells in the peripheral and central nervous system, but also includes blood cells and cells at the joint level that may affect pain pathways indirectly. Pre-clinical and clinical data suggest that modulation of mitochondrial functions can be used to attenuate or eliminate pain, which could be beneficial for multiple rheumatic diseases.

Acute pain is a prevalent symptomatology in prehospital emergency care. Although inadequate assessment and treatment of acute pain are associated with various complications, about 43% of adults suffering from pain are undertreated. This phenomenon is poorly studied, and limited data are available in the literature. The objective was to investigate the pain management in a prehospital emergency health-care setting, verifying pain assessment, pharmacological treatment adherence and the effectiveness of pain relief therapy.

The watching of films is popular and accessible to broad segments of the population. The depiction of medical conditions in films has the potential to affect the public's perception of them and contribute to stereotypes and stigma. We investigated how patients with chronic pain and their management are depicted in feature films. Films that contained characters with or references to chronic pain were searched for using databases such as the International Movie Database. Themes that emerged from the content analysis revolved around the films' depictions of characters with pain, their health care providers, and therapies for pain management. Patients with chronic pain were depicted in various ways, including in manners that could elicit empathy from audiences or that might contribute to the development of negative stereotypes about them. The attitudes of health care professionals toward patients with chronic pain ranged from compassionate to dispassionate. Pain management was typically depicted as lacking in breadth or using multidisciplinary approaches with a focus on pharmacological management. The variety of topics related to chronic pain depicted in feature films lends to their use in medical education strategies to better inform health care professions trainees about chronic pain management.

Functional abdominal pain disorders (FAPDs) are common gastrointestinal problems in children, and the pathophysiology is thought to be multifactorial. Adverse early life events (ELE) induce alterations in the central nervous system, perhaps predisposing individuals to develop FAPDs. We aimed to study the potential adverse ELE that are associated with FAPDs.

Using data from all those born in a single week in 1958 in Britain we track associations between short pain and chronic pain in mid-life (age 44) and subsequent health, wellbeing and labor market outcomes in later life. We focus on data taken at age 50 in 2008, when the Great Recession hit and then five years later at age 55 in 2013 and again at age 62 in 2021 during the Covid pandemic. We find those suffering both short-term and chronic pain at age 44 continue to report pain and poor general health in their 50s and 60s. However, the associations are much stronger for those with chronic pain. Furthermore, chronic pain at age 44 is associated with a range of poor mental health outcomes, pessimism about the future and joblessness at age 55 whereas short-duration pain at age 44 is not. Pain has strong predictive power for pain later in life: pain in childhood predicts pain in mid-life, even when one controls for pain in early adulthood. Pain appears to reflect other vulnerabilities as we find that chronic pain at age 44 predicts whether or not a respondent has Covid nearly twenty years later.

Speaker gender representation at medical conferences is a significant site of gender disparity. Our primary objective was to quantify the proportion of female speakers and compare plenary session opportunities by gender at the North American Neuromodulation Society (NANS) Annual Conference.