Russian Article

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Russian Article

Postby mrhodes40 » Sun Jul 12, 2009 3:19 pm

I asked Dr Simka if he had seen a Russian article that i had read about and the good doctor got a copy and translated it from Russian. He thought a copy would be helpful so that we can link it for other medical people to the research thread :D . KEEP COMMENTS ON TOPIC. Thanks!


Ogleznev KO, Tsuladze II
Department of Neurosurgery, Moscow, Russia
Diagnosis of venous circulatory disorders in the cervical portion of the spine and cord by selective phlebography.
Vestnik Rentgenologii i Radiologii, 1993


Abstract
Selective phlebography of the major branches of the superior caval vein, supplemented, in necessary, by selective catheterization of the vertebral vein, was employed to study the disorders in the cervical section of the spine and cord. Twenty-five patients with myelopathies of obscure origin were examined. The ,main symptoms were stenoses and atresias of the orifices of the internal jugular veins and compression and stenoses of the brachiocephalic veins. The possibility of a reverse venous blood stream from the non-spinal veins to the epidural ones and backward was confirmed. Therefore, a disorder of the venous outflow from the vertebral canal, on the one hand, and intensification of the venous blood flow, on the other, may develop under certain conditions, resulting in hypertension inside vertebral canal. Eight patients with pathologic changes in the veins were operated on (decompression and angiolysis).


Fig. 1 – the scheme of major tributaries of the superior caval vein and venous system of vertebral column: 1 – superior caval vein, 2 – brachiocephalic vein, 3- internal jugular vein, 4- anterior epicondylar vein, 5 - vertebral vein, 6 – epidural venous system

Fig.2 - stenosis of right internal jugular vein

Fig. 3 -occlusion of left internal jugular vein

Fig. 4 - retrosternal stenosis of left brachiocephaliuc vein


Diseases of major venous trunks can result in the disturbances of vertebral venous system. This leads to the elevation of venous pressure in the vertebral canal and to the chronic venous stasis in this area.
Anatomy of the vertebral venous system and its connection with major intravertebral veins has been described years ago. There are also well known principles of venous outflow from the cerebral cavity, and venous hemodynamics of cervical spine and spinal cord. However, these data have not been yet applied to clinical practice.
There are often seen neurologic patients, whose clinical picture does not fit to any of classic diagnosis, and therefore they need further testing.
It is well known that ligature of the both internal jugular veins is not followed by an evident pathology. It is also known that after the Queckenstedt manoeuvre during lumbar puncture (pressure on jugular veins) the subarachnoid space is reduced due to enlargement of the epidural space resulting from a dilation of the vertebral epidural venous plexus, which in turn increases the pressure of cerebrospinal liquid. Moreover, it has been proven experimentally that venous outflow from the brain is dependent on a position of the body. In the horizontal position blood outflows through internal jugular veins, and in the upright position through the vertebral epidural venous plexus.
Thus, it could be said that there exist two outflow ways from the brain: internal jugular veins and vertebral epidural venous plexus. But the role of the latter is underestimated.

Material and methods.
(There is a detailed description of selective venography of assessed veins; rather technical issues).

Results.
In a case of unclear clinical picture, and no clear characteristics and localization of spinal cord pathology, patients were diagnosed with venography. Selective venography was performed in 25 patients with clinical diagnosis of: “myelopathy of unclear origin”. There were 15 male and 12 female patients, they were aged 30-61 years (mean age 45 y). In addition, 2 patients were examined with angiography of carotid arteries, 12 patients – CT and MRI, 6 patients – with myelography, 18 patients – with lumbar puncture.
Stenosed parts of veins were usually found above of behind the clavicle, and these stenoses were 3 cm long. In a case of venous atresion, the remaining part of the vein was significantly dilated and it looked like a gigantic aneurysm. During injection of the contrast dye, the turbulent flow was visible, and sometimes it led to contrasting of the entire blood vessel. In our opinion, these turbulences resulted from a forced blood flow through stenosed vessel. This, in turn, resulted in high venous pressure above the stricture and in subsequent vessel dilation. Maximal diameter of the vein was 2 to 5 cm.
In some cases internal jugular veins were entirely filled with contrast dye and, moreover, contrast dye was even seen in the vertebral epidural venous plexus. Such a contrasting of vertebral epidural venous plexus is the sign of the reversed venous outflow from the jugular vein towards cranial cavity. In other patients, however, contrast dye stayed only at the site of injection, irrespective of the speed of the injection. These findings seam to be related to velocity of reversed venous flow, venous pressure and severity of pathologic process. In all cases of pathologic stenoses of internal jugular veins, contrast dye stayed in the vein for 10-15 seconds, even up to several minutes.
There are only casuistic papers on the role for brachiocephalic veins in the pathogenesis of spinal cord symptoms and pathologic venous circulation. Therefore, we have focused on these pathologies. There were stenoses and compressions of the brachiocephalic veins. Stenoses were found retrosternally or in the space between clavicle and 1st rib. Stenoses in the retrosternal portion were associated with deformation of the vein and reversed flow in the left vertebral vein. This led to hypertension in the distal part of the brachiocephalic vein with subsequent blood flow towards vertebral canal. Compression and stenosis of the brachiocephalic vein between clavicle and 1st rib resulted in hypertension in the internal jugular vein. This in turn resulted in the venous outflow from the cranial cavity through vertebral epidural venous plexus, which was seen during venography.
Control group comprised of 30 patients who were done selective vertebral venography for other reasons (discopathy, neoplasms of spinal cord, traumatic lesions to brachial nervous plexus). Vertebral epidural venous plexus was contrasted during the selective venography of vertebral veins, and these vessels could be visualized from the middle part of cervical spine to the middle part of thoracic spine. This phenomenon can be explained by the fact that the blood velocity in the epidural venous plexus was higher that that of injected contrast dye. After the speed of injection of the dye was increased to 4 ml/s, epidural venous plexus could be visualized at the entire length of cervical spine and, moreover, contrast dye could been also seen within internal jugular veins. Such a contrasting of vertebral epidural venous plexus via internal jugular veins, and vice versa, confirms the possibility of a reversed venous blood flow.
Thus, in a case of lesions in the internal jugular veins and brachiocephalic veins, the venous outflow from vertebral canal is maintained through vertebral veins and, moreover, the blood flow through vertebral veins is increased, which leads to overloading of these vessels and to venous hypertension inside the vertebral canal.
Apart from the above-described signs of venous hypertension inside the vertebral canal, we have shown some signs of disturbed venous circulation in the bones. These signs result from a dilated vertebral epidural venous plexus and vertebral veins. The latter become tortuous. The right superior intercostals vein, which drains the upper part of the vertebral canal, becomes dilated. Dilation of this vein can be explained by an increased function, and on venograms it is seen as enormously developed vessels, which can be visualized from the beginning of the vein to its junction with the azygous vein. We could seen such a vein in all examined patients.
There were also indirect signs of venous lesions, such as the presence of rich collateral network with anastomoses within muscles and subcutaneous tissue. The presence of collaterals shows that the capacity of vertebral epidural venous plexus passes the limit and the additional amount of blood is redirected into collateral pathways. This, in our opinion, is the cause of pains in the neck and occipital area, and also the cause of variable sensory disorders.
It should be emphasized that pathology of major tributaries of the superior caval vein has been found in 22 of 25 examined patients, and in 17 cases there was pathology of the internal jugular vein. These were: stenosis at proximal part of left internal jugular vein: 6 cases, stenosis at proximal part of right internal jugular vein: 3 cases, occlusion at proximal part of right internal jugular vein: 5 cases, occlusion at proximal part of left internal jugular vein: 2 cases. In 3 cases there were both occlusion and stenosis of a vein. In 5 patients there were pathologies of brachiocephalic veins: in 3 cases – stenosis of left brachiocephalic vein (in one case in the retrosternal segment of the vein), and in 2 patients there was compression of the vein between 1st rib and clavicle (in one case the compression was seen bilaterally).
Eight patients were operated on: 6 patients because of the lesions in the proximal internal jugular veins, and 2 patients because of the lesions of brachiocephalic veins. Operative treatments consisted of decompression of bony lesions and of liberation of the vein. We are optimistic that the results of surgical treatment indicate that such a management is promising and should be continued in the future.

Conclusions.
1. Selective venography can reveal lesions in the major tributaries of the superior caval vein, which seam to be the principal cause of disturbed venous outflow from the vertebral canal, but on the other hand result in an increased inflow of venous blood into the vertebral canal.
2. Selective venography can reveal reversed venous flow from the internal jugular vein to the vertebral epidural venous plexus, and vice versa. This can explain the development of venous hypertension inside the vertebral canal. This explains also a disturbed venous outflow from the vertebral canal in the presence of such lesions.
3. The role of the vertebral epidural venous plexus, which serves purpose of a collateral outflow pathway, in the maintaining of venous outflow from the cranial cavity is equivalent to that of the internal jugular veins.
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Postby mrhodes40 » Sun Jul 12, 2009 8:03 pm

I'm having computer issues so I can't be here too much--it's on life support I'm afraid :lol:

Ok I want to point out a few things:

Twenty-five patients with myelopathies of obscure origin were examined

These patients had myelopathies so this was presenting as problems with the spinal cord leading to neurological problems, but it was not specifically "MS".
The ,main symptoms were stenoses and atresias of the orifices of the internal jugular veins and compression and stenoses of the brachiocephalic veins. The possibility of a reverse venous blood stream from the non-spinal veins to the epidural ones and backward was confirmed.

The problems seen were blockage of the jugulars or brachiocephalic veins. Based on how the anatomy is and where the veins go they assumed that this would result in reflux or reverse blood flow into the veins directly adjacent to the spine. When they did the studies they confirmed that this was true: these blockages caused problems via the venous system for the spine.
Therefore, a disorder of the venous outflow from the vertebral canal, on the one hand, and intensification of the venous blood flow, on the other, may develop under certain conditions, resulting in hypertension inside vertebral canal

Because of the way the venous system is this results in high venous pressure in the spinal area, i tis kind of a double whammy.
Diseases of major venous trunks can result in the disturbances of vertebral venous system. This leads to the elevation of venous pressure in the vertebral canal and to the chronic venous stasis in this area.
Anatomy of the vertebral venous system and its connection with major intravertebral veins has been described years ago. There are also well known principles of venous outflow from the cerebral cavity, and venous hemodynamics of cervical spine and spinal cord. However, these data have not been yet applied to clinical practice.

They are essentially outlining venous stasis, the same pathology we see in legs, in the cerebral system and saying that although this stuff is known facts about the venous system as it pertains to the head, WE DON'T TREAT PEOPLE BASED ON THESE PRINCIPLES YET. 1993 folks.
It is well known that ligature of the both internal jugular veins is not followed by an evident pathology. It is also known that after the Queckenstedt manoeuvre during lumbar puncture (pressure on jugular veins) the subarachnoid space is reduced due to enlargement of the epidural space resulting from a dilation of the vertebral epidural venous plexus, which in turn increases the pressure of cerebrospinal liquid

This section says that though it is thought that jugular veins can be occluded and no damage occurs, we already know because of this quickenstadt thing that there is increased pressure on the spine when you do that. They are kind of questioning the assumption that jugs can be blocked without harm.

In some cases internal jugular veins were entirely filled with contrast dye and, moreover, contrast dye was even seen in the vertebral epidural venous plexus. Such a contrasting of vertebral epidural venous plexus is the sign of the reversed venous outflow from the jugular vein towards cranial cavity.

This section is discussing the outcome of the venograms and saying that when they injected dye into the jugs it went into the spine area and also there was a significant amount of reflux and chaotic blood flow. It also was clear that the blood was regurgitating towards the brain
In all cases of pathologic stenoses of internal jugular veins, contrast dye stayed in the vein for 10-15 seconds, even up to several minutes.

Is it ANY WONDER WE GET HOT when the brain is cooled through the emissary veins? when the mechanism to cool the brain is to eject the hot blood through the venous system which included through the jugs?
There are only casuistic papers on the role for brachiocephalic veins in the pathogenesis of spinal cord symptoms and pathologic venous circulation. Therefore, we have focused on these pathologies. There were stenoses and compressions of the brachiocephalic veins. Stenoses were found retrosternally or in the space between clavicle and 1st rib. Stenoses in the retrosternal portion were associated with deformation of the vein and reversed flow in the left vertebral vein. This led to hypertension in the distal part of the brachiocephalic vein with subsequent blood flow towards vertebral canal. Compression and stenosis of the brachiocephalic vein between clavicle and 1st rib resulted in hypertension in the internal jugular vein. This in turn resulted in the venous outflow from the cranial cavity through vertebral epidural venous plexus, which was seen during venography.

A similar wacky blood flow pathology with the brachiocephalic stenosis
Thus, in a case of lesions in the internal jugular veins and brachiocephalic veins, the venous outflow from vertebral canal is maintained through vertebral veins and, moreover, the blood flow through vertebral veins is increased, which leads to overloading of these vessels and to venous hypertension inside the vertebral canal

That says it all these stenoses resulted in overloaded veins
There were also indirect signs of venous lesions, such as the presence of rich collateral network with anastomoses within muscles and subcutaneous tissue. The presence of collaterals shows that the capacity of vertebral epidural venous plexus passes the limit and the additional amount of blood is redirected into collateral pathways. This, in our opinion, is the cause of pains in the neck and occipital area, and also the cause of variable sensory disorders.

They are essentially saying if the collaterals are present then this shows that the capacity has been overloaded and is the cause of these problems in these patients.

This is an incredible concurrence with the paradigm that Dr Zamboni has offered in his work. In Russia. In 1993.

I was talking with my sister and she commented that because most of our research is funded by pharmaceutical companies and this is not pharmaceutical by nature it is just not going to get noticed or picked up as a project by people. They have to get funding or they can't study something like this. She said they used to have a lot of money for "unfunded research" but that has dried up over the years for some reason, the unfunded pot is small. She's a college admin.

So 1993 in Russia they were already aware of this. In the 80's Dr Schelling put out his book.

THANK GOD this is being looked at NOW.
Please do discuss this..... :wink:
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Postby cheerleader » Mon Jul 13, 2009 5:07 am

Sorry you're having computer issues, Marie. Hope you get that taken care of....I'm on a PC here in FLorida. wow. miss my Mac :)
First question, where are the brachiocephalic veins, and how do they play into the CNS?

Second question...I could only think of Island Girl when reading this....

There were also indirect signs of venous lesions, such as the presence of rich collateral network with anastomoses within muscles and subcutaneous tissue. The presence of collaterals shows that the capacity of vertebral epidural venous plexus passes the limit and the additional amount of blood is redirected into collateral pathways. This, in our opinion, is the cause of pains in the neck and occipital area, and also the cause of variable sensory disorders.


What's an anastomoses? Jeff had tons of collaterols we could see, but no neck pain. Could there be collaterols forming within muscle tissue that are not detected on Dr. Dake's MRVs? Are we looking at enough veins now at Stanford?

whatcha think?
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby mrhodes40 » Mon Jul 13, 2009 5:44 am

The brachiocephalic gathers the jugular and subclavian blood and dumps to the vena cava.

and an anastomosis is a channel, a hole, a connection, between two things that does not ordinarily belong there and that allows something to communicate between these areas.

I thought that about IG too, but I assume that Dr D would have noticed any rich network of such collaterals or anastasmoses if they had been there as he did a venogram. She did have that anomaly at the brachiocephalic that was too small to be a stenosis, but may be as more is learned things of that nature will be seen in a different light.

that having been said these in this paper were fairly significant not mild, you can tell by the references to the amount of turbulence seen on the venograms and the size of the tortuosities etc.

but it confirms that these venous anomalies can cause neurological symptoms through venous hypertension.
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
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Postby Sharon » Mon Jul 13, 2009 1:08 pm

Some of this sounds like me -

from Dake's report:

Repeat venography of the left jugular system demonstrates a valve at the junction with left brachiocephalic vein with narrowed segments inferior to the stented segment. After placement of stent in the location and venoplasty, the pressure gradient improved.....wtih relief of narrowing.


I have two stents - the big one in the left jugular, and then the one described above which was placed overlapping and distal to the big stent.
The pressure gradient did not improve when the first (big) stent was placed. It was improved after the second stent was placed.

Also,
Superior vena cavagram demonstrates reflux into the asygous system. Asygous venography demonstrates no evidence for stenosis, with small branches which appear to demonstrte antegrad flow draining from superior location. There is no pressure gradient from the asygous to the superior vena cave.


I need to reread your post - lots of information and I am kind of slow on this medical jargon :wink:
Sharon
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Postby Jamie » Mon Jul 13, 2009 1:42 pm

Wow.

Have you sent this to Dr. Dake?
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Postby mrhodes40 » Mon Jul 13, 2009 2:35 pm

Yes, of course! :D :D :D :D
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
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Postby Vonna » Sat Jan 09, 2010 12:28 pm

Hello,
I know I'm chiming in a little late, but just wanted to say thank you for posting this. Very interesting. It just validated Dr. Zamboni more.

I agree that most of our research is funded through pharmaceutical, therefore, what can we expect but more drugs?

The more I read about CCSVI, the more sense it makes. I can't help but think this has been right under the researchers' noses for so long. Why did we have to wait till now to find this out?
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Postby cheerleader » Sat Jan 09, 2010 12:43 pm

Welcome, Vonna. Thank you so much for reviving this wonderful thread. Posts like this one from Marie are what make TIMS so vital. Yes, the connections to the vasculature are finally being made by doctors in a variety of practices. Here is a wonderful article from Dr. Mark Haacke on the history of the venous connection to MS-

http://www.ms-mri.com/history.php
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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