This Is MS Multiple Sclerosis Community: Knowledge & Support

Hi Dr. Have there been discussions about valve repair or replacement at any of the meetings of the CCSVI Leaders. I was wondering if at your Symposium or the SIRs meetings or whether Dr Zamboni had looked at what difference it could make to the reflux/back jet issues. There would be discussion on positioning of replacements no doubt.
Although it would be new technique it still has to be considered I would guess.
The multiple Angio treatments would appear to be missing stopping the reflux long term, the flow may improve but there is always going to be reflux risk and no peace of mind that the issues that cause symptoms of MS are rectified.
Regards Nigel

Hi, Dr Sclafani
You will see herunder two reports : scanner and MRI.
I don't know if you could tell something more.
The conclusion of my vascular surgeon (absolutly not aware of ccsvi) was : no stenose on jugular veins, reduced diamater was due to a reduced lateral venous sinus, congenital, nothing to do ...
Of course, I can't be satisfied with a such answer.
Is it nessecary to do others exams like a Doppler protocol Zamboni ?
How to check azygos vein ? I have a medular MS.
What do you think ?
Many thanks

CT-scan NECK
INDICATION:
Evaluation of a size asymmetry of the jugular veins.
TECHNIQUE
Purchase volume focuses on the regions of the brain, cervical and upper thoracic, immediately after intravenous injection of contrast. (DLP = 1283.25 mGy-cm)
RESULTS:
The exploration of the brain parenchyma does not show any abnormal density or abnormal enhancement.
No detectable defect size branches of Polygon of Willis.
The superior longitudinal veinous sinus opacified satisfactorily and drains almost entirely into the right lateral sinus.
The jugular foramen measured 73 mm2 right, left 36 mm2.
It confirms the size asymmetry of the jugular veins, the right jugular vein has a surface of 48 mm2 to 145 mm2.
The left jugular vein has an axial surface at least 15 mm2 compared to the anterior border of the lateral process of C2 and the posterior border of the styloid process (pictures 357-400 series 2).
The maximum size of the left jugular vein was measured at 95 mm2.
This asymmetry of size seems to be related to the size asymmetry of lateral venous sinus, although the recess between the C2 of the styloid process has a low antero-posterior diameter (4 mm).
Moreover, the subclavian veins in the innominate vein have a normal size.
It is not viewed abnormal opacification of the aortic arch (the left vertebral artery arises directly from the aortic arch).
No abnormal contrast enhancement visible in the light of the upper aero-digestive tract.
Integrity of the thyroid and salivary glands.
No adénomégalie lateral cervical spinal or supraclavicular.
No obvious change of the lung apex.
No mediastinal mass syndrome higher.
CONCLUSION:
Asymmetry confirmed for the jugular veins with a size asymmetry of constitutional lateral intracranial venous sinuses.

MRI ANGIO-AND VENOUS BLOOD OF THE CERVICAL REGION
INDICATION:
Review of headache.
TECHNICAL:
Sagittal Tl Axial FLAIR, diffusion, axial gadolinium Tl centered on the brain. Angio-MRI with gadolinium injection centered in the cervical region during the arterial and venous time.
RESULT:
1 - Brain: Presence of two punctiform hyperintense T2 FLAIR infra-tentorial.
In Supratentorial, we visualize a beach on T2 subcortical left temporal, 12 mm long axis associated with a hyperintense cortical than 4 mm in diameter and 4 mm right frontal peri-ventricular diameter front left. These violations do not enhance démyélmisantes during injection of contrast, compliance with apparent diffusion coefficient.
2 - Neck: No obvious abnormality of the aortic arch. Birth of the left vertebral artery directly from the aortic arch. The supra-aortic arteries are of normal size and signal abnormalities without their weapons. No anomaly visible gauge of the branches of the circle of Willis.
The venous vascular exploration of the neck size of the asymmetry found in appearance congenital sinus venous side with a predominance of right side.
It still looks laminate the left jugular vein high in its course without real retro-styloid extrinsic compression or intraluminal signal abnormality.
The subclavian vein and innominate venous trunks are of satisfactory size and permeability.
CONCLUSION:
Presence of some demyelinating infra and supra-tentorial and does not enhance on injection of contrast.
Size asymmetry of the jugular veins of congenital pace without significant extrinsic compression.

In my case, yes, a vein pinched by a muscle definitely does grow collaterals. My venogram images of my RIJV look like there's a spider web of collaterals surrounding the vein, which is impinged by a muscle bundle.

The presence of collaterals alone does not indicate reflux, though. According to Cheerleader, one of her husbands stents has closed up, but a collateral has formed bypassing it that is allowing for adequate drainage.

So, again, I'm left wondering why most IRS seem to be treating every area of stenosis they come across, regardless of blood flow turbulence?

_________________
Marc
www.wheelchairkamikaze.com

Marc in addition to your comments I wonder if there is reflux issues that occur when we are actively moving around, all the tests are all done in passive positions?
The natural thought would be that reflux must happen in situations where body positions 'crimp' blood flow in veins that have normal flow, the question would need to be what role do valves play, how important are functioning valves?
The difference between standing and lying down is only a small part of the function of blood return flow with the jugulars involvement. The other veins are needing to be understood better before the picture is understood.
The incidence of collaterals at the thyroid is a case in point. The thyroid function has connection to most MS symptoms. Disruption of flow at the thyroid is another area of concern.
If a stent closes or restenosis occurs then reflux is likely to occur also, the question would be how long does the process of developing alternative flow take? How long before the slow flow causes damage?
This leads me back to my favorite point, could one way valves solve issues caused by slow flow and reflux?

Marc, thanks for the information, I had wondered back with the CTOS discussions about this (if the muscle would pinch off collaterals from being grown too.)

I think it is perhaps inflammatory to suggest that most IRS are stenting every area of stenosis? Dr. Sclafani has been quite clear that he will not stent, Dr. Siskin only stents when he sees it as absolutely necessary which is in a small minority of cases.

I will read with interest when Dr. Sclafani weighs in on this. My thought is that reflux is not the entirety of the problem. Or the "pathophysiology of the entity," which hurts to type. It's the diversion of all this blood flow, that should be going down a strong healthy jugular with thick walls, into these collaterals with weak leaky walls that aren't meant to do the job they've been made to do. Plus the stasis or moment of diversion when the blood hits the obstruction and goes off into the collaterals will weaken the endothelium thereabouts. But Zamboni himself has weighed in on your case and thought it did not need treating. It is hard to argue with Dr. Zamboni. But even he does not know the entirety of this discovery yet.

Here also (I am no expert) is the Zamboni criteria, for a doppler diagnosis of CCSVI. Reflux is mentioned in two of them, but it is possible to have a diagnosis without reflux. A 3 & a 4 or a 3 & a 5?

I misstated in my previous post. I should have said most IRS are treating every stenosis they see, not stenting. There is definitely a lot more ballooning than stenting going on. I'll actually go back and change that through the edit function now.

_________________
Marc
www.wheelchairkamikaze.com

marc, nigel and cece
your questions and comments deserve more than i can give at 134am. I will return to discuss further tomorrow
s

Thanks Dr. get some rest please.

Dr. S,

The positional statement of SIR came out sometime back. It was then endorsed by the Canadian SIR. How exactly is the SIR hierarchy organized? Does the statement issued by SIR mean that in general there is a consencus around the world on this? Does this need to be carried to local SIR's?

Just trying to understand ...

_________________
A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it
- Max Planck

I would think another way for CCSVI to do damage without causing reflux is if the obstructions slow down the flow of blood, reducing the cerebral perfusion of the brain, which is known in MS to be reduced.

To demolish my earlier point, if an obstruction is low enough down, leaky walls in the collateral or near the obstruction shouldn't matter much, since it wouldn't be leaking onto brain tissue. Hmm.

A question of my own: in CCSVI, why might a jugular have an abnormally high flow velocity?

Cece,

I was thinking the same.....the bloodflow has to be at a constant speed. Like the gas-'flow' in a car. The engine will hick-up or go wild if the flow is slowing down or speeding up..it doesn't have to be a reflux to cause problems.

Just my thoughts......

Robert

Dear Cece,

Here is my take on reflux

I agree with you that CCSVI problably causes damage without refux. I think that refux is simply an indication that there is an obstruction further downstream and an attempt by the complicated and elaborate venous system to bypass the obstruction. The presence of reflux may, however, be an indication of the severity of the obstruction. When obstruction is severe enough the blood will sometimes have to reverse direction and find an alternative route out. This is what the reflux is.

Does reflux by itself cause direct damage? I really do not think so. I think it only causes damge if flow in the refluxing vein ends up being reduced and affects the flow in the small vessels (capillaries and venules) draining into it. I think that as long as there is continous flow in the small vessels (even with reflux) the CNS should be ok. I think that what is particularly destructive is a reduction in the rate of flow. Stasis (or absent flow) would be worse than reflux. If the rate of flow in the larger vessels or refuxing vessels is reduced, then there will be reduced flow in the smaller vessel because they cannot drain into the larger ones adequately. I think this is key to understanding how CCSVI can cause neurological symptoms. It is the smaller vessels that are intimately involved with and affect the functioning of brain tissue. Neurological deficits have to somehow be mediated through the smaller vessels and endothelium, as mentioned in Cheerleaders endothelial health article. Reduced flow in smaller vessels causes ischemia of brain tissue, activates the coagulation and inflammatory cascade and evenutally causes breakdown of the blood-brain barrier and causes plaques.

North

Endothelial defect/weakness could also explain the differences observed - Whether stenosis or not... Or am I just confabulating here?

My understanding is that reflux is a key component to the CCSVI hypothesis, in that it explains the breakdown in the blood brain barrier that allows for the immunological response that is a hallmark of MS. A simple reduction in blood flow, while certainly capable of doing harm to the CNS over the course of decades, would not explain the infiltration of T cells into the CNS, as is proven by the presence of O-bands in the CSF of MS patients. Reflux, resulting in a breakdown of the BBB, would account for the inflammation seen in RRMS; a long-term reduction in overall blood flow likely would not. If CCSVI is to eventually be determined to be a causal factor in MS, it must play a role in the breakdown of the BBB.

It seems that many "pro" CCSVI researchers (among them Dr. Zivadinov at the BNAC) are beginning to come to the conclusion that CCSVI is certainly associated with MS, and plays a role in the severity and progression of the disease, but is looking less likely to be a causal factor.

If you read my recent blog post on CCSVI, there are several paragraphs that summarize Dr. Z's presentations at ECTRIMS. To ensure that I wasn't misstating his conclusions, my contacts at BNAC, who I consulted while doing research for the piece, requested that he get a chance to look over the pertinent paragraphs before I published them. Of course, I agreed, and the paragraphs came back with only very minor changes, none of which involved the conclusions drawn.

Of course, even if CCSVI is not a causal factor in the etiology of MS, the discovery of its association with the disease remains a major breakthrough and paradigm shifting idea.

_________________
Marc
www.wheelchairkamikaze.com

I have now heard this several times, in the form that MS patients have reduced blood transit time in the brain. Is this correct, and do you know where that research can be found?