Full paper online, for free.
Here, we present a comprehensive review of the pathophysiology of MS, ADEM, pseudotumor cerebri, and optic neuritis, with an emphasis on the roles of venous vascular system programming and dysfunction in their pathogenesis. We consider the fundamental differences between arterial and venous endothelium, their dissimilar responses to inflammation, and the potential theoretical contributions of venous insufficiency in the pathogenesis of neurovascular diseases.
Unlike the cerebral arterial system, the spatial organization of cerebral venous networks is more complex and more often asymmetric, with greater structural heterogeneity than cerebral arterial anatomy. Consequently, this half of the circulatory system has been far less studied and understood .
The concept that neurologic disease can be influenced by structural or functional abnormalities of the CNS venous system has raised intense worldwide debate among researchers, with many investigators arguing against its existence. Controlled, careful clinical studies are needed to validate when and how vascular alterations can contribute to forms of CNS injury and inflammation. Here, we provide a discussion on the potential pathogenesis of these diseases, with emphasis on venous endothelial dysfunction in MS, ADEM, and other forms of neuroinflammation.
There has been less research into the arterial and venous differences in MS. Despite these limitations, vascular contributions in MS do appear to support the notion of the vasculature being an initiating target in MS etiology and not simply a bystander presentation of other disease processes. Perhaps the strongest support for this is the number of MS therapies that have been developed, which target leukocyte binding to activated endothelial cells, a central component of the blood-brain barrier (BBB).
It's a good one.
Thanks to Shayk for sending this along to me today---