CCSVI in MS reviews
Posted: Fri Aug 17, 2018 2:07 am
CCSVI theory is not dead. Just looking for its place in the big picture.
Neuroinflammation (book). Review.
Chapter 29 - The Contribution of Extra Cranial Venous Drainage to Neuro-Inflammation in Multiple Sclerosis
https://www.sciencedirect.com/science/a ... 7095000363
Abstract
The role of the extracranial veins in the pathogenesis of inflammatory neurological/neurodegenerative diseases remains largely unknown and under-investigated.
A condition named chronic cerebrospinal venous insufficiency (CCSVI) strikes the main extracranial veins and determines a slight increase in pressure up to the brain venules. The condition is linked with a recently-described chain of pathophysiologic events. Impaired CSF diffusion into the brain parenchyma between the peri-arterial and the perivenous spaces contributes to a worsened protein clearance.
Furthermore, restricted venous outflow through the jugular veins reduces perfusion and the energy available to oligodendrocytes for myelin synthesis. Both peptide waste and myelin debris represent a strong chemotactic signaling. Increased transmural pressure in the CCSVI condition may also facilitate blood-brain barrier leakage and red blood cells extravasation. Consequently, iron stores are increased and likely linked to inflammation and degeneration.
The contribution of the impaired venous function to neuroinflammation/degeneration warrants further studies in this direction.
Neuroinflammation (book). Review.
Chapter 29 - The Contribution of Extra Cranial Venous Drainage to Neuro-Inflammation in Multiple Sclerosis
https://www.sciencedirect.com/science/a ... 7095000363
Abstract
The role of the extracranial veins in the pathogenesis of inflammatory neurological/neurodegenerative diseases remains largely unknown and under-investigated.
A condition named chronic cerebrospinal venous insufficiency (CCSVI) strikes the main extracranial veins and determines a slight increase in pressure up to the brain venules. The condition is linked with a recently-described chain of pathophysiologic events. Impaired CSF diffusion into the brain parenchyma between the peri-arterial and the perivenous spaces contributes to a worsened protein clearance.
Furthermore, restricted venous outflow through the jugular veins reduces perfusion and the energy available to oligodendrocytes for myelin synthesis. Both peptide waste and myelin debris represent a strong chemotactic signaling. Increased transmural pressure in the CCSVI condition may also facilitate blood-brain barrier leakage and red blood cells extravasation. Consequently, iron stores are increased and likely linked to inflammation and degeneration.
The contribution of the impaired venous function to neuroinflammation/degeneration warrants further studies in this direction.