septums

[Cece]

http://onlinelibrary.wiley.com/doi/10.1 ... aintenance

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.

This was in the external jugular veins. If there are publications on septums in the IJVs, I have not found them. If we have a septum in an EJV, it might divert some flow to the IJV, which might cause a problem if the IJV is blocked. But I thought this was interesting because it states that the septum is composed of tunica intima and tunica media, as compared to the venous valves that are composed of tunica intima only.

Here is a definition of tunica media, which is found in septums:

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]

http://en.wikipedia.org/wiki/Tunica_media

The Cleveland autopsy study found more septums than I would have expected, based on the very low number of people here at TiMS who can say they were diagnosed with a septum, and suggesting that septums may be getting misdiagnosed as valves. This is concerning if the septums are of different composition and might require different treatment than a valve or have a different prognosis. Intravascular ultrasound is one way to differentiate between a septum and a valve.
http://registration.akm.ch/einsicht.php ... KEN_ID=900

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.

www.ccsvi.org/index.php/the-basics/glossary
CCSVI Alliance provides this definition of a septum.

[ttucker3]

One impact of hypoxia on veins is agiogenesis (blood vessel creation). I perceive that hypoxia is the probable primary trigger for collateral vein growth. Some IRs (Arata, Sclafani for example) seem to be saying that valve malfunction is the primary malformation that they observe. Is is a possibility that observed IJV malformations like flaps, septums, webs, etc may be a consequence of agiogenesis which is in turn a consequence of hypoxia from an incompetent valve? Do these observed IJV malformations occur in patients many years after initial MS diagnosis, giving the needed time for collatoral or other malformation growth?

Trev Tucker

[cheerleader]

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.
Highly recommend this paper:
http://fondazionehilarescere.org/pdf/03-2518-ANGY.pdf

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.

perhaps chaotic flow, hemodynamic changes and hypoxic injury turn a relatively benign malformation into a real problem? Budd Chiari takes decades to destory a liver....
cheer

cheer

[ttucker3]

Thanks cheer - more reading in store. I note my typo (not once but twice) angiogenesis no agiogenesis.

Trev. Tucker

[Cece]

Is CCSVI creating a hypoxic situation for veins, as well as our brains? It seems reasonable.
Here's an article on venous hypoxia:
http://content.karger.com/produktedb/pr ... =000320624

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].

Do our jugular veins have a vasa vasorum network supporting them?
(Vasa vasorum: http://en.wikipedia.org/wiki/Vasa_vasorum )

I cannot find much about septums in blood vessels. Here is something on angiogenesis causing vascular malformations to worsen. It is not clear if it is truncular or extratruncular vascular malformations, which is a significant difference.

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.''

http://www.childrenshospital.org/az/Sit ... 830P5.html

[DrCumming]

For some "easy" reading see

http://www.theodora.com/anatomy/develop ... ystem.html

it would make sense that these abnormal valves and septums are a result of something going wrong during the formation of the venous system.

[Cece]

You have a high opinion of us, when you call that easy reading.

Here's an interactive embryology diagram that I found useful too. It's similar to figures 477 - 480 in the link that Dr. Cumming posted.

http://www.embryology.ch/anglais/pcardio/venen01.html

(Click on 'start' at the bottom and watch the veins differentiate.
#6, the superior cardinal vein in blue, is the one that becomes the IJV and subclavian and others.
#20 is the azygous, from the orange supracardinal vein)

[DrCumming]

that's cool. would like to find one like that for everything above the heart up to the brain!

[1eye]

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.

I think collateral growth is known to be a natural reaction to a shortage of oxygen in the blood: after all, even veins need it to live. So that would agree with Dr. Zivadinov's finding, which I still consider a "smoking gun" that MS people have more collaterals, indicating they are suffering from hypoxia. Did we know that already? Are skeptics saying it ain't so, or that it doesn't come from CCSVI? I think them being around the jugulars is a pretty good clue.