This Is MS Multiple Sclerosis Knowledge & Support Community

Abstract
We examined 70 external jugular veins from 35 cadavers. In six veins we observed a septum, 6–25 mm long, which completely divided the lumen of the vein. The septum, which has not been previously described, was located approximately 5 cm superior to the vein's termination into the subclavian vein. Histologically, the septum is composed of tunica intima and tunica media in contrast to venous valves which are composed of tunica intima only.

The middle coat [tunica media] is composed of a thick layer of connective tissue with elastic fibers, intermixed, in some veins, with a transverse layer of muscular tissue. [4]

Septum
A wall-like formation of tissue inside the vein. Abnormally located septum(s) may block or inhibit blood flow through a vein. In particular, Dr. Zamboni et al. describe septum/valve malformations specifically at the point where the internal jugular veins connect with the Superior Vena Cava.

The truncular venous malformation (VM) represents an embryologically defective vein where developmental arrest has occurred during the vascular trunk formation period in the ‘later stage’ of the embryonic development. A relatively simple truncular VM lesion such as a venous web at the hepatic venous outlet causes portal hypertension giving a profound damage/impact to the liver. A similar condition involving the head and neck venous system may cause chronic cerebro-spinal venous insufficiency (CCSVI) and may be involved in the development or exacerbation of multiple sclerosis.

Inadequate oxygen supply from luminal blood or vasa vasorum or both could potentially cause vein wall hypoxia. Two mechanisms, both related to blood stasis and venous hypertension, have been proposed to cause hypoxia to the varicose vein wall:

(1) Endoluminal hypoxia: stagnation of venous blood flow results in reduced oxygen replenishment in comparison to normal venous flow. Endothelial and inner layers of the vein wall are first affected in endoluminal hypoxia [16,17,18].

(2) Medial hypoxia: distension of the vein by hydrostatic pressure secondary to blood stasis causes compression of vasa vasorum. Therefore, the media and outer layers of the vein wall are first affected [17,18].

A VM is caused by errors that occur when blood vessels are forming, and our investigators are currently probing the genes and molecules that regulate the formation and growth of blood vessels. Understanding the genes that control these molecular events will hopefully result in new therapies for vascular malformations.

New treatment for venous malformations?

Venous malformations can sometimes grow, requiring aggressive treatment to protect your child's health. Research at Children's has shown that urine testing can help monitor VMs and predict those about to become a serious threat.

These findings suggest that angiogenesis (the formation of new blood vessels) plays a role in the progression of vascular malformations, raising the possibility of curbing these difficult-to-treat anomalies with anti-angiogenic drugs.

''Prior to this study, we had thought it was not possible to treat vascular malformations with drugs, since congenital anomalies generally do not respond to drugs,'' says Steven Fishman, MD, a surgeon on Children's Vascular Anomalies team. ''This study gives us hope that with further research we'll be able to develop drug treatments.''

Interesting posit on collateral growth, Dr. Tucker.
As far as septum being created later in the disease process-Dr. B.B. Lee discusses the congenital nature of septum malformations, as they are involved in Budd-Chiari.