Dr. Coen at ISNVD

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Dr. Coen at ISNVD

Postby Cece » Tue Feb 21, 2012 1:46 pm

page 50
Collagen Expression in Neck Brain Draining Veins (Matteo Coen, SWITZERLAND)

Venous anomalies have been associated with different neurological conditions and the presence of a vascular
involvement in multiple sclerosis (MS) has long been ascertained. In view of the recent debate regarding the
existence of cerebral venous outflow impairment in MS due to anomalies of the azygos or internal jugular veins
(IJVs), we have studied the morphological and biological features of brain draining veins in MS patients. We
examined: 1) IJVs specimens (N=5) from MS patients with diagnosis of chronic cerebrovascular venous
insufficiency who underwent surgical reconstruction of the IJV, as well as specimens of the great saphenous
vein (N=2) used for surgical reconstruction; 2) different vein specimens (N=9) from a MS patient dead of an
unrelated cause; and 3) autoptical and surgical IJV specimens (N=10) from patients without MS. Collagen
deposition was assessed by means of Sirius red staining followed by polarized light examination. The
expression of collagen type I and III, cytoskeletal proteins (α-smooth muscle actin and smooth muscle myosin
heavy chains), inflammatory markers (CD3 and CD68) were investigated. The extracranial veins of MS patients
showed focal thickenings of the wall characterized by a prevailing yellow-green birefringence (corresponding
to thin, loosely packed collagen fibers) correlated to a higher expression of type III collagen. No differences in
cytoskeletal protein and inflammatory marker expression were observed. The IJVs of MS patients presenting a
focal thickening of the vein wall are characterized by the prevalence of loosely packed type III collagen fibers in
the adventitia.
The role of this finding in MS pathogenesis needs further testing.
This gets away from looking at imaging of jugular veins and involves looking at actual jugular veins, removed at autopsy or during surgical reconstruction. If inflammatory marker expression was not observed, does that mean that the thickening of the jugular veins was not due to inflammation? The collagen in our veins is different than the collagen in the veins of healthy controls. One question is if we began this way or if these collagen differences are a result of chronic reflux in these veins.
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