Simka Marian
Department of Vascular & Endovascular Surgery, Euromedic Specialist Clinics, Katowice, Poland.
Rev Recent Clin Trials. 2012 May;7(2):93-9. doi: 10.2174/157488712800100198.
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.
在奇静脉和颈内静脉中发现狭窄，即伴随多发性硬化症的所谓慢性脑脊髓静脉功能不全，使得人们能够重新解读关于这种神经系统疾病的知识。中枢神经系统病理性静脉流出似乎会导致两个主要问题。首先，它会破坏血脑屏障，并可能使谷氨酸和白细胞穿透神经实质。其次，它可能导致大脑和脊髓严重灌注不足。这两种重叠的病理状况可能通过半胱天冬酶-1驱动的少突胶质细胞焦亡引发斑块，并通过谷氨酸兴奋性毒性引发神经退行性变。此外，脑灌注不足可能导致慢性疲劳和其他全身性神经症状。希望这篇综述将有助于阐明多发性硬化症的新策略和治疗方法，并为这种使人衰弱的疾病的研究展示新的途径。
