Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The discovery of stenoses in the azygous and internal jugular veins, the so-called chronic cerebrospinal venous insufficiency that accompanies multiple sclerosis, has enabled the reinterpretation of knowledge about this neurologic disease. Pathologic venous outflow from the central nervous system appears to lead to two main problems. Firstly, it disassembles the blood-brain barrier and may allow the penetration of nervous parenchyma by glutamate and leukocytes. Secondly, it may result in significant hypoperfusion of the brain and spinal cord. These two overlapping pathologies are likely to trigger plaques through caspase-1-driven pyroptosis of oligodendrocytes and to evoke neurodegeneration via glutamate excitotoxicity. Moreover, brain hypoperfusion may lead to chronic fatigue and other global neurologic symptoms. It is hoped that this review will help to elucidate new strategies and treatments for multiple sclerosis and will show new avenues for the research on this debilitating disease.
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PMID:Possible pathomechanisms responsible for injury to the central nervous system in the settings of chronic cerebrospinal venous insufficiency. 2235 41

Accumulated evidence suggests that cardiovascular autonomic nervous system (ANS) dysfunction may be the underlying cause of many MS clinical presentations, including neurodegeneration and reduced response to immunomodulatory therapies, depression, fatigue and sleep disorders, migraine, osteoporosis, and chronic cerebrospinal venous insufficiency, the newer MS vascular etiology. We have recently described the genetic, epigenetic, and environmental factors with the potential influencing ANS activity, and the interactions among these factors. This review expands upon previous ones, describing the pharmacological, non-pharmacological, and surgical strategies that could be adopted to prevent and minimize the deterioration in ANS function, promoting a state of sympathovagal balance. However, these strategies should not be applied as "one size fits all", but should take into account the nature and the degree of ANS dysfunction. These strategies would be effective in improving ANS function not only in MS, but also in other autoimmune and neurodegenerative diseases, where the dysfunction of this system plays a role.
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PMID:Promoting sympathovagal balance in multiple sclerosis; pharmacological, non-pharmacological, and surgical strategies. 2594 28

Objective Chronic cerebrospinal venous insufficiency (CCSVI) has been hypothesized to be a risk factor for multiple sclerosis (MS). Venoplasty has been proposed as a treatment for CCSVI. The aim of our study was to gain a better understanding of the "real-world" safety and longitudinal effectiveness of venoplasty Methods: British Columbia residents who self-reported having had venoplasty and consented to participate in the study were interviewed and followed for up to 24 months post-therapy using standardized structured questionnaires Results: Participants reported procedure-related complications (11.5%) and complications within the first month after the procedure (17.3%). Initially, more than 40% of participants perceived that the venoplasty had had positive effects on their health conditions, such as fatigue, numbness, balance, concentration/memory and mobility. However, this improvement was not maintained over time Conclusions: Follow-up patient-reported outcomes indicated that the initial perception of the positive impact of venoplasty on the health conditions of MS patients was not sustained over time. In addition, venoplasty was not without associated morbidity.
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PMID:Patient-Reported Benefits of Extracranial Venous Therapy: British Columbia CCSVI Registry. 2827 Feb 50

The prevalence and incidence of chronic venous leg ulcers (CVLUs) are increasing worldwide, as are the associated financial costs. Although it has long been known that their underlying etiology is venous insufficiency, the molecular aspects of healing versus nonhealing, as well as the psychoneurologic symptoms (PNS; pain, cognitive dysfunction, fatigue, depression, and anxiety) associated with CVLUs remain understudied. In this biobehaviorally focused review, we aim to elucidate the complex mechanisms that link the biological and molecular aspects of CLVUs with their PNS. Innovations in "omics" research have increased our understanding of important wound microenvironmental factors (e.g., inflammation, microbial pathogenic biofilm, epigenetic processes) that may adversely alter the wound bed's molecular milieu so that microbes evade immune detection. Although these molecular factors are not singularly responsible for wound healing, they are major components of wound development, nonhealing, and PNS that, until now, have not been amenable to systematic study, especially over time. Further, this review explores our current understanding of the molecular mechanisms by which the immune activation that contributes to the development and persistence of CVLUs also leads to the development, persistence, and severity of wound-related PNS. We also make recommendations for future research that will expand the field of biobehavioral wound science. Biobehavioral research that focuses on the interrelated mechanisms of PNS will lead to symptom-management interventions that improve quality of life for the population burdened by CVLUs.
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PMID:Biobehavioral Mechanisms Associated With Nonhealing Wounds and Psychoneurologic Symptoms (Pain, Cognitive Dysfunction, Fatigue, Depression, and Anxiety) in Older Individuals With Chronic Venous Leg Ulcers. 3114 48


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