Abstract
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.
Keywords: Axonal injury, azygous vein, blood-brain barrier, caspase 1, glutamate, jugular veins, multiple sclerosis, venous insufficiency
Reviews on Recent Clinical Trials
Title:Possible Pathomechanisms Responsible for Injury to the Central Nervous System in the Settings of Chronic Cerebrospinal Venous Insufficiency
Volume: 7 Issue: 2
Author(s): Marian Simka
Affiliation:
Keywords: Axonal injury, azygous vein, blood-brain barrier, caspase 1, glutamate, jugular veins, multiple sclerosis, venous insufficiency
Abstract: 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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Cite this article as:
Simka Marian, Possible Pathomechanisms Responsible for Injury to the Central Nervous System in the Settings of Chronic Cerebrospinal Venous Insufficiency, Reviews on Recent Clinical Trials 2012; 7 (2) . https://dx.doi.org/10.2174/157488712800100198
DOI https://dx.doi.org/10.2174/157488712800100198 |
Print ISSN 1574-8871 |
Publisher Name Bentham Science Publisher |
Online ISSN 1876-1038 |
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