This Is MS Multiple Sclerosis Knowledge & Support Community

I cant help but giggle at their loose use of the term "healthy controls", since they were DEAD!

But they were very healthy dead people. I hope I'm very healthy when I die, as long as it is from natural causes.

And, once dead, I hope I stay that way, even if I am healthy...

drsclafani wrote:

Cece wrote:

Marked valvular and other intraluminal abnormalities with potential hemodynamic consequences were identified in 5 of 7 MS patients (7 abnormalities) and in 1 of 6 controls (1 abnormality). These abnormalities included circumferential membranous structures (1 MS and 1 control), longitudinally-oriented membranous structures (3 MS), single valve flap replacing IJV valve (2 MS), and enlarged and malpositioned valve leaflets (1 MS). In addition, minor anatomic variations without expected hemodynamic consequences were observed similarly in both MS and controls. These included valves with >2 leaflets, the presence of valves in the AZY, additional (duplicate) normal-appearing IJV valves, and small membranous septa.

This is excellent. Since we are looking at visible structural abnormalities, it is hard to argue with autopsy results.

They found more of the longitudinally-oriented membranous structures (aka septums) than what we usually hear about here. Perhaps these are underdiagnosed in patients? Could they be missed on IVUS?

Perhaps it is what we call elongated valves.
Perhaps some of the images interpreted as valves are septums. I think so.
perhaps with flow the septum is collapsed against the wall during venography and not visible.

A single valve flap replacing IJV valve might be how you'd describe my left jugular issue, unless it were better described as an enlarged valve leaflet. Finding only three valve abnormalities total in seven MS patients (14 jugulars) is fewer than what the IRs are seeing in living patients.

It is likely that autopsy is going to miss many of the malfunctioning valves because they fixed the tissue. Thus they are seeing only anatomical derangements, but not seeing mobility challenges. Many of the valvular problems seen with IVUS represent immobile valves. During a real time physiological analysis, one seems that the valve opens incompletely and the stenosis is present. I do not think that autopsy will detect these problems.

But this is clear support of the association between CCSVI intraluminal abnormalities and MS. It also helps clarify why there might be so much difficulty finding CCSVI, if the imaging studies are failing to differentiate between venous wall stenoses, which were found equally in both the MS patients and controls, and the intraluminal abnormalities, which were overwhelmingly found in the MS patients.

therefore emphasizing the importance of a real time intraluminal interrogation of the veins with IVUS.

There are always things I did not think of, which you have.
I agree with all of this.
If some images are being interpreted as valves but are really septums, that is going to affect outcome of those procedures, if valves are more responsive to treatment than septums are. (Although IVUS is, as usual, the solution.)

Just a simple observation. The original study said:

"The incidence of vein wall stenoses was similar in MS and controls: eight stenoses in 4 of 7 MS patients and five in 3 of 6 controls."

A simple way of re-stating that would be that roughly half (4/7) of the pwms had 8 stenoses and roughly half (3/6) of controls had 5 stenoses. That is almost a doubling of the number of stenoses in pwms. Now I accept this is a very small sample and I do not know what tests of significance they may have applied. But to me this data does not seem to support their assertion that the incidence was similar in both groups. The trend is clearly for pwms to have more stenoses.

Dr. Zamboni has always said-
"It is not about architecture, it is about flow."
When someone is dead, you can see the structure of the vein, or the architecture, but not the flow.
It is the intraluminal defects (which were in 5 out of 7 pwMS and only one control) that affect flow.
Stenosis is just architecture.....the intraluminal defects that change flow, and that's what matters.
cheer

Stenosis == narrowing == less diameter.

To achieve the same flow with a narrower diameter, you need to increase the pressure. Higher pressure means upstream stresses increase, and vein walls may weaken, as well as the BBB.

Architecture is something else. I would call it the big picture i.e. total number of vessels, average diameter, number and size for each function, etc. I think the statement makes sense if you are trying to argue against CCSVI by saying the neck veins have enough redundancy and capacity for collateral growth that you don't need jugulars.

I think it would be interesting to see if postmortem results back up what Zivadinov is saying about capillaries.

to increase flow .... you need to increase the SPEED of the PUMP.

PUMPS create FLOW .

RESISTANCE to flow ......creates PRESSURE.

This can be read on page one of any hydraulic manual. Or you can simply accept
my explanation .It will save you a lot of time.

The heart is a pump. A fluid pump. Your brain is the equipment it runs . This "master " runs all the other components . Arms . Legs . Lungs. Do I need to go on ?

Reducing or stopping fluid flow INTO the'' master " ...... has dire consequences . Stroke. Death.

Reducing or stopping fluid flow " OUT " of the master ..... has consequences also.... MS ?

Ask any Hydraulic Engineer , what happens to a circuit , when the " return side " is not capable of carrying flow......

Answer : Every F---ing thing grinds to a halt ......

That my friends ....... is CCSVI.


Understand ?



Mr.Success

MrSuccess wrote:to increase flow .... you need to increase the SPEED of the PUMP.

PUMPS create FLOW .

RESISTANCE to flow ......creates PRESSURE.

This can be read on page one of any hydraulic manual. Or you can simply accept
my explanation .It will save you a lot of time.

The heart is a pump. A fluid pump. Your brain is the equipment it runs . This "master " runs all the other components . Arms . Legs . Lungs. Do I need to go on ?

Reducing or stopping fluid flow INTO the'' master " ...... has dire consequences . Stroke. Death.

Reducing or stopping fluid flow " OUT " of the master ..... has consequences also.... MS ?

Ask any Hydraulic Engineer , what happens to a circuit , when the " return side " is not capable of carrying flow......

Answer : Every F---ing thing grinds to a halt ......

That my friends ....... is CCSVI.


Understand ?



Mr.Success

I love mechanical analogies.

To me the brain is like a fuel-burning engine, with the arteries supplying the fuel and the veins carrying away the exhaust. For maximum performance you need an efficient fuel delivery system and good exhaust flow. If you stick a sock in the exhaust pipe of your car, it will soon behave like it has MS. It will drive around like weak sauce and may even sputter sputter and stall. Pull out the sock, the engine will recover, and Bob's your uncle.

I just wish some of these neuro's would stick a sock in it.

My simple understanding is that it may not just be a question of flow. Back in the early days of CCSVI, there was a lot of talk (generally coming from Dr Simka I think) regarding the effects of non-laminar flow on the permeability of the BBB.

I would be guessing that anti CCSVI advocates would say that the total flow is not reduced, but the rate of flow is simply increased, not stopped or even really reduced.

Won't reflux affect shear stress? I think they are saying it may, and that this could be bad for the BBB. Why are MS veins disappearing? Maybe the effect of the higher pressure pre the stenosis is causing more shear stress in the veins upstream.

Shear stress seems very important in blood. We think we know how shear affects blood vessels, and at the site of a defect there may be more shear. They are calling it "reactionary remodeling of affected blood vessels. "

I think Dr. Simka wrote about how shear also affects the stuff that makes leukocytes stick to blood vessels. I thought (wrongly?) that since it is a low pressure system there might not be any turbulence. I guess maybe though it's a lower value normally, maybe veins are more sensitive to shear than arteries, and a change can have a much greater effect. Idle speculation.

I found out, along the way that blood viscosity varies as expected with temperature. But because hematocrit (number of red cells) and vessel diameter (capillaries are different) affect viscosity, the temperature/viscosity relationship is not easy for me to figure out.

also found this
--------TRANSLATION:

Your brain isn't going to get enough blood gases (oxygen and nitrogen) if your blood is too thick.

Particularly interesting is the conclusion hematocrit may affect viscosity and perfusion in brain.

Under physiological conditions and reduced whole blood viscosity, plasma viscosity may play a tissue-dependent relevant role. The role of plasma viscosity might become crucial in organs that normally autoregulate, such as the heart, kidney and the brain, when vasomotion is impaired by vascular damage.
Increases of overall viscosity above normal baseline values should be avoided under pathological conditions in the brain and elsewhere – all situations where vascular autoregulatory mechanisms are inoperative due to ischemia, structural damage or physiologic dysfunction.

also ---- TRANSLATION:
If you have a vein problem, leading to your brain, you will be affected by temperature, and by thickening blood, caused by sugar/carbs, and as we just read, hematocrit (iron is the main part of this).

Julie Stachowiak, Ph.D. was at the ECTRIMS presentation of Dr. Fox, and writes about it here:
http://ms.about.com/b/2011/10/25/a-ccsv ... r=facebook

I find it ironic that when a neurologist notes intraluminal defects, it is a breakthrough, yet when Dr. Zamboni wrote and researched and published on these same malformations, it was lunacy.

At least the tide is turning.....if neurologists can find and recognize venous malformations that have hemodynamic affects, we are getting there...
cheer

good link to Julie Stachowiak . A must read .

And I found the comments from Dr.Arata [ after the article ] most informative .

As for Colin Rose ........ it's really hard to take someone's opinion seriously that writes a health blog that rants and raves about the ''evils of potatoe chips " , and any other thing he suspects lives under his bed or closet ....... read his bumpf ... more or less for amusement. I suspect he will be writing his damning articles in crayon in the near future .

I think he's nuts.


Good job Julie Stachowiak .


Mr.Success

Dr. Arata mentioned the difference between his early understanding of CCSVI as narrowed veins, versus his more recent understanding of the CCSVI as a flow disorder primarily due to abnormal valves. Yet this was already in Dr. Zamboni's work. This is from 2009.

As for the jugular veins, they were found to be stenosed unilaterally or bilaterally in 59/65 patients (91%). The stenoses were frequently annulus and septum, followed by atresia; no twisting was observed (fig 2B (f, g, h)).

http://jnnp.bmj.com/content/80/4/392.full
Annulus, meaning the ring of the valves.

a comment on a comment ........ I read that Colin Rose still takes the position that having CCSVI would result in an immense pressure within the head. [ read his comments that follow the Julie Stachowiak article ]. No wonder Rose cannot understand CCSVI , he does not understand how blood flows OUT OF THE HEART.

The heart is a fluid pump. That's it's purpose. It moves fluid [blood] in small volumes. Each heart beat fills the arteries that connect to it. The cartoid arteries are the blood pipeline to the brain. When the brain reaches full volume of blood - fluid flow is diverted to other artery pathways . IT DOES NOT CONTINUE TO POUND BLOOD INTO YOUR BRAIN .

Our hearts are a diaphram pump ... NOT a positive displacement pump ... as Rose erronously would have you to believe.

The condition CCSVI allows for blood to enter and exit the brain ..... but slower.

As I have said before , speeding up the pump [ running , jumping , fear ..... ] increases the FLOW of the blood ...... I suspect the collaterals support the increase ...

Is this why physical exercise seems to help with MS symptoms ?


It's as good a theory as any others ..........



Mr. Success

MrSuccess wrote:all of this is not possible if not for the foresight and courage of those that have donated their body to science. We cannot thank them enough . They are true hero's.


Mr.Success

You're right about that. I wonder if there is a way we can donate our bodies specifically for CCSVI research.

I hope though that all the answers will have been found before anymore of us kick the bucket.