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That last article was the best one. Really interesting. Venous distensibility is the same as venous elasticity, unless I'm using the terms wrong, and elasticity is one of the factors Dr. Tucker was using in his equations. He said that venous elasticity was reduced in women compared to men. Migraine sufferers are also predominantly female.

Bed rest is a way to increase venous distensibility. Lowering intravascular pressure increases distensibility. Hypertension reduces it, which is not good.

One of the things some doctors check, when encountering a narrowing, is if it expands under Valsalva. If it is distensible, in other words. I don't think the Taiwanese doctors are describing stenotic veins, that wouldn't distend at all, but rather veins that distend less than normal veins would.

Veins lose elasticity as they age. But migraines get better as people age (fewer, less painful migraines that don't last as long). That is not explained.

I would think the endothelial health program would be excellent for this! It makes me want to adhere more closely to it myself.

http://books.google.com/books?id=1duFI8 ... ty&f=false

Vascular Distensibility
Blood vessels are elastic, which means they can be distended by raising intravascular pressure or diminished in radius by lowering it. This fact does not alter any of the principles already discussed; the ratio of driving pressure to flow still depends on length, radius, and other variables, as indicated in equation 6.3 The one new phenomenon in distensible tubes is that transmural pressure, the difference between the pressures inside and outside the vessel, is now one of the factors that control the radius. Extravascular, or interstitial space, pressure is 0 to 3 mm Hg under most conditions, much lower than intravascular pressure. The elasticity of the blood vessel walls plays a large role in hemodynamics for two reasons. First, the contraction or relaxation of vascular smooth muscle alters vessel diameter by changing the elasticity of the wall. Second, the elasticity of a vascular bed determines how much blood volume is accommodated within that region at the existing local pressure.

On page 186 of the same text, it defines distensibility, which is synonymous with compliance.

OK, just so Joe Layman (me) can understand: now let's say patients with migraines have less compliant IJVs. What does that mean? Near as I can tell: less compliant means like stiffer, harder, less elastic as you say. That would mean less likely to balloon out under pressure. In the case of veins with higher pressure at one end, less likely to balloon out at the other end. It seems that maybe what is happening, is some people have less elastic IJVs, pressure upstream, in the brain. That is going to result in ballooning outward of the veins upstream if they have more normal elasticity. Pressure has to have an outlet. If veins upstream are not going to bleed, they have to balloon outward, or comply. They have to not be as stiff. Result: pressure on other things surrounding the veins. Maybe at weaker spots (junctions?) the smaller ones become more permeable and it becomes more likely that things that shouldn't, filter through. Lets say you have a screen, with holes designed to keep a certain size object on one side. Now stretch the screen. What happens? More of that size object gets through the screen.

Now some people who may get headaches that aren't migraines, just bad headaches, have stiff jugulars, similarly non-stiff veins, venules, and capillaries upstream, in the head, but they have a permanent narrowing in those stiff jugulars. The formerly artificially higher pressure becomes permanently higher, and things have to change. Collateral veins develop. Ballooning outward upstream becomes more permanent. The blood does not have as much throughput, if not enough collateral veins develop, soon enough. Less oxygen and food get through because stuff upstream uses it all up. Maybe capillaries starve and are resorbed. Maybe the stiff jugulars get even stiffer.

I speculate that the difference between migraine people and other people with stiff IJVs is that there is more normal pressure upstream in the migraine sufferers, because there is no narrowing. If you artificially narrow the stiff jugulars by applying pressure, there is artificially more upstream pressure, and the normal brain veins upstream, artificially balloon outward, putting more pressure on them, which might result in artificial leaking, if you kept doing it long enough. If the person had a headache, it just might get artificially worse.

So where is CCSVI? The migraine sufferers don't have the narrowing of CCSVI but do have stiff jugulars, so they occasionally get enough upstream pressure to cause ballooning, and headaches from that, but the blood doesn't slow down enough to lose all that oxygen and food and the ballooning goes away, because the upstream veins resume their original shape and the pressure reduction makes the headaches go away.

But why don't the people with the narrowing get headaches? Well, some research (M. Freedman, et. al) says they actually do, more than normal people, but they also have blood-brain barrier leakage, less blood throughput, some chronic oxygen/food starvation, resorption of capillaries, atrophy of brain parenchyma volume, loss of axons and myelin due to the BBB leaks, which result in too many leukocytes. Maybe in some, the chronic lack of blood/food/oxygen throughput actually makes more veins upstream of the stenosis stiffer. And a few other things.

OK, so my name's not Joe.

Veins lose elasticity as they age. But migraines get better as people age (fewer, less painful migraines that don't last as long). That is not explained.

I think we are looking at elasticity of some veins with respect to others. Ones that are closer to the surface, to the air, might be more likely to become drier, and stiffer. Internal jugulars may be more internal than other veins, but still more external than veins, venules and capillaries inside the skull. Just a thought.

Besides, if veins inside the skull distend less, aren't they less likely to affect the other stuff trying to share that space, and less likely to cause headaches?

OK--found the earlier publication from the same researchers on venous flow and migraine, it clarifies what they were looking at---
http://www.ncbi.nlm.nih.gov/pubmed/21317790

Abstract
OBJECTIVE:
We aimed to assess whether migraine is associated with changes in the distribution of the venous drainage through primary and secondary pathways by using phase-contrast magnetic resonance imaging (MRI).
METHODS:
We examined 26 patients (37.3 ± 13.9 years) with recurring migraine headaches and 26 age- and gender-matched controls with no neurologic disease (37.3 ± 13.7 years) on a 3 Tesla MR scanner. A 2D time-of-flight MR-venography of the upper neck region was performed to visualize the venous vasculature. Cine-phase contrast scans with high-velocity encoding were employed to quantify arterial inflow and flow in the primary venous channels (right and left jugular veins), whereas scans with low-velocity encoding were employed to quantify flow in the secondary venous channels (epidural, vertebral, and deep cervical veins).
RESULTS:
Patients with migraine showed (i) a higher prevalence of dense secondary extracranial venous networks (15 vs. 2, P = 0.00002) and (ii) a significantly larger percentage of venous outflow through secondary channels (10.5% vs. 5.5%; of total cerebral blood flow, P = 0.02). This mainly included drainage through epidural, vertebral, and deep cervical veins.
CONCLUSION:
Migraine patients showed a significantly larger percentage of venous outflow through secondary channels. The mechanism of this alteration remains to be elucidated. Potential mechanisms include repeated release of vasoactive substances or growth factors.

I think decreased venous distendability might be a reason for the main usage of the collateral network, rather than the jugulars...but is this truly a secondary situation, as these researchers imply, or could this lack of distendability be primary, created in utero- due to something like a collagen disorder like Ehler Danlos?

Again, this is NOT CCSVI, but it is an interesting correlation in altered blood flow and a neurological condition that is related to white matter lesions in the brain. Very interesting!
cheer

Ok, now I've heard 2 things, besides that the primaries are the jugs, and the secondaries are the verebrals (the case when you are lying down, but not when standing - were any of these MRVs done upright?). One, that in migraine the jugs are stiff, and two, that there are also "dense" secondaries, i.e. if anybody is talking about collaterals, it is not around the jugulars. That implies no stenosis in the jugulars.

Maybe, the jugs are already stiff, because something in their environment, or their heredity, is making them that way, and collaterals don't grow very well there, but the more internal routes work better, are more amenable to secondary growth, and don't get as stiff.

cheerleader wrote:OK--found the earlier publication from the same researchers on venous flow and migraine, it clarifies what they were looking at---
http://www.ncbi.nlm.nih.gov/pubmed/21317790

Abstract
OBJECTIVE:
We aimed to assess whether migraine is associated with changes in the distribution of the venous drainage through primary and secondary pathways by using phase-contrast magnetic resonance imaging (MRI).
METHODS:
We examined 26 patients (37.3 ± 13.9 years) with recurring migraine headaches and 26 age- and gender-matched controls with no neurologic disease (37.3 ± 13.7 years) on a 3 Tesla MR scanner. A 2D time-of-flight MR-venography of the upper neck region was performed to visualize the venous vasculature. Cine-phase contrast scans with high-velocity encoding were employed to quantify arterial inflow and flow in the primary venous channels (right and left jugular veins), whereas scans with low-velocity encoding were employed to quantify flow in the secondary venous channels (epidural, vertebral, and deep cervical veins).
RESULTS:
Patients with migraine showed (i) a higher prevalence of dense secondary extracranial venous networks (15 vs. 2, P = 0.00002) and (ii) a significantly larger percentage of venous outflow through secondary channels (10.5% vs. 5.5%; of total cerebral blood flow, P = 0.02). This mainly included drainage through epidural, vertebral, and deep cervical veins.
CONCLUSION:
Migraine patients showed a significantly larger percentage of venous outflow through secondary channels. The mechanism of this alteration remains to be elucidated. Potential mechanisms include repeated release of vasoactive substances or growth factors.

I think decreased venous distendability might be a reason for the main usage of the collateral network, rather than the jugulars...but is this truly a secondary situation, as these researchers imply, or could this lack of distendability be primary, created in utero- due to something like a collagen disorder like Ehler Danlos?

Again, this is NOT CCSVI, but it is an interesting correlation in altered blood flow and a neurological condition that is related to white matter lesions in the brain. Very interesting!
cheer

Excellent, that explains what is meant by primary or secondary channels. Ok, in this one too they're proposing the use of collaterals rather than jugulars to be a secondary result of and not a primary cause of migraines, but they don't have the information we have about the lack of distensibility of the jugulars as seen in the Taiwanese research, and they might not be taking outflow abnormalities too seriously or think there is a way for the outflow abnormality to affect the brain upstream. We however have plenty of reason to believe that outflow abnormalities can affect the brain.

I'm not ready to hazard a guess as to the cause of a lack of distensibility in the jugulars in the migraine patients. We need some autopsy data on migraine patients, with samples of their jugulars, to check for collagen levels. We have this for CCSVI patients, who show abnormalities in the collagen (with more collagen III instead of collagen I).

I would want to know if ballooning the length of the jugulars would improve the distensibility, which could relieve migraines.

I need a lab of my own.... I don't think there are any researchers out there who are going to delve into this, yet. Some migraine sufferers have sought CCSVI treatment, if my memory serves.

http://www.eurekalert.org/pub_releases/ ... 020210.php

Migraine more common in women with MS


ST. PAUL, Minn. – Migraine is seen more frequently in women with multiple sclerosis (MS) than those without, according to a study released today that will be presented at the American Academy of Neurology's 62nd Annual Meeting in Toronto April 10 to April 17, 2010.

"While having a history of migraine diagnosis was linked to MS, women with migraine need to know that over 99 percent of them will never develop MS, thus having migraine should definitely not be a reason to worry about getting MS," said study author Ilya Kister, MD, with New York University School of Medicine and a member of the American Academy of Neurology. "More research is needed since it's still not known whether migraine is a risk factor for developing MS or if it is a condition that occurs at the same time as MS."

The study involved 116,678 women who were part of the Nurses' Health Study II. Of these women, 18,000 had been diagnosed with migraine at the start of the study. The women were followed every two years for 16 years. During the study, 375 women were diagnosed with MS. Of those, 82 had reported at the beginning of the study that they had been diagnosed by a doctor with migraine.

The study found that women with a migraine diagnosis at the beginning of the study were 47 percent more likely to develop MS than women without a diagnosis. The results were the same regardless of age, where they lived, Scandinavian ancestry, vitamin D levels, smoking status and body mass index.

The research represents the first large scale study of its kind to explore the relationship between migraine and MS.

More data on this relationship will be presented by Kister at the American Academy of Neurology Annual Meeting in Toronto.

Hmmmm!!

http://neurologique.blogspot.com/2010/0 ... ccsvi.html

Think about the name of a diagnosis that affects women more than men; young more than old; has a genetic component; normal appearing white matter may not be so normal; has white spots (T2 hyperintensities) on brain MRI in a quarter of people in some series; and involves inflammation on the meninges (covering of the brain, optic nerves and spinal cord).

Give up?

Clue: It's not MS.

It's migraine.

http://www.msworld.org/forum/showthread.php?t=110300

I can add that my wife had the [CCSVI] procedure two months ago, and one of the benefits has been that her migraines have reduced in both frequency and severity.....she is able to stop most of her headaches now with just advil or tylanol
she used to have to take fioracet (sp?) a proscription almost everyday

So there may be a connection......at least in her case

a patient's report from another forum

1eye wrote:I speculate that the difference between migraine people and other people with stiff IJVs is that there is more normal pressure upstream in the migraine sufferers, because there is no narrowing. If you artificially narrow the stiff jugulars by applying pressure, there is artificially more upstream pressure, and the normal brain veins upstream, artificially balloon outward, putting more pressure on them, which might result in artificial leaking, if you kept doing it long enough. If the person had a headache, it just might get artificially worse.

So where is CCSVI? The migraine sufferers don't have the narrowing of CCSVI but do have stiff jugulars, so they occasionally get enough upstream pressure to cause ballooning, and headaches from that, but the blood doesn't slow down enough to lose all that oxygen and food and the ballooning goes away, because the upstream veins resume their original shape and the pressure reduction makes the headaches go away.

But why don't the people with the narrowing get headaches? Well, some research (M. Freedman, et. al) says they actually do, more than normal people, but they also have blood-brain barrier leakage, less blood throughput, some chronic oxygen/food starvation, resorption of capillaries, atrophy of brain parenchyma volume, loss of axons and myelin due to the BBB leaks, which result in too many leukocytes. Maybe in some, the chronic lack of blood/food/oxygen throughput actually makes more veins upstream of the stenosis stiffer. And a few other things.

OK, so my name's not Joe.

Interesting, 1eye. One of my questions from Dr. Zamboni's autopsy/valve graft data on actual CCSVI jugulars was if the collagen abnormalities seen were limited to the area of the valve or were throughout the jugular. If it's throughout the jugular, then do we have stiff jugulars too?

So, Cece, you see (see?) we are slightly at odds about this:

That last article was the best one. Really interesting. Venous distensibility is the same as venous elasticity, unless I'm using the terms wrong, and elasticity is one of the factors Dr. Tucker was using in his equations. He said that venous elasticity was reduced in women compared to men. Migraine sufferers are also predominantly female.

Bed rest is a way to increase venous distensibility. Lowering intravascular pressure increases distensibility. Hypertension reduces it, which is not good.

One of the things some doctors check, when encountering a narrowing, is if it expands under Valsalva. If it is distensible, in other words. I don't think the Taiwanese doctors are describing stenotic veins, that wouldn't distend at all, but rather veins that distend less than normal veins would.

Veins lose elasticity as they age. But migraines get better as people age (fewer, less painful migraines that don't last as long). That is not explained.

I would think the endothelial health program would be excellent for this! It makes me want to adhere more closely to it myself.

I think there must be some difference between veins in the head and elsewhere. I still have not had any answer I can trust about whether veins in the head have no smooth muscle layer. Hypertension is indeed, not good. But it existing means different things between veins and arteries, and depending on whether or not they are in the brain, which is encased in the skull, where distension, or ballooning outward, as I have been calling it, means increased pressure on everything else. Where it encounters the push-back from non-compressible fluids (like around ventricles) encased in bone, it means increased fluid resistance and viscosity, which will also tend to slow down circulation. One of the things which will have much more stress on it is the endothelium in the hypertense brain. So that may be why the lesions (and the BBB leakages?) are peri-ventricular. I think something that increases stiffness in brain veins may indeed be good (like age). I do not think better elasticity (distensability) is a good thing (promoted by bed-rest). Because the fluid inside and outside of a vein is non-compressible, the endothelium , insofar as it is compressible will compress, and insofar as it will stretch, other compressible matter outside the veins and ventricles will also have to compress (atrophy?).

Maybe that is another reason why bed-rest in "MS"/CCSVI is not such a good thing. Not only do we not have the widened jugulars, which normal supine posture would bring, and the stenosis impeding normal jugular flow when supine, but it increases elasticity upstream, where the only thing allowed to compress is the brain-matter.

When I was about eight, Mr. Wizard came on the television, and said that if you filled a glass bottle, and capped it, underwater, so that it was entirely filled with water, and all the air was gone, you could use the bottle as a hammer, and drive a nail with it. I did this, and found it was true. The non-compressible water made the bottle as hard as a rock. It took throwing it high in the air over a hard road surface to break it, which made it also similar to a rock. But you could drive a nail, and not break the glass, partly because the glass, while harder than a bottle with some air in it, was flexible compared to a capped bottle full of water, with no air in it. It would distend and flex enough not to let the nail break through it. Don't try this with a cork, though, as it will probably compress, and the bottle will break. Glass will cut your hand. The bottle that hit the road shattered into long shards, the shape of which was very unexpected, and very sharp.

Cece

Thanks for the vote of confidence and your understanding of the proposition I am putting forward about the role of venous/venule hypertension and vein compliance. I am hoping there will be some face to face discussion in Orlando with those who have more fluid dynamics than I, particularly combined with medical and imaging knowledge. I am particularly looking forward to Michael Markls presentation on the future of 4D flow quantification. Raj Attariwala is also someone to pay attention to. As for me, I am a simple rocket scientist who can read literature. I think we need a broad range of disciplines working together, including someone who possesses Navier-Stokes analysis/simulation tools to help reveal the origins of MS. I also think the ISNVD holds great promise for offering this collaboration. Last year's show in Bologna was a superb start.

Trev. Tucker

Footnote: My son has MS and my daughter-in-law has migraines. Let's get a solution before my grandsons get to their mid-teens.

1eye

My perception is that, under the condition of venous hypertension, if the vein is more compliant then it is able to expand more under the influence of the same amount of pressure than if it is less compliant. This greater expansion reduces the pressure that is ultimately built up. If for example the vein were entirely rigid (inflexible) the total pressure would be the sum of the pressures of the direct and reflux pulses). However, if the vein is able to expand the pressure build-up will be less than if it were unable to expand. My expectation is that the product of pressure*volume will be approximately the same for rigid and compliant veins. Hence, if volume becomes greater the required pressure is less. Where this leads is that female veins being about 50% less compliant than male veins means one would expect greater hypertension in women and hence, greater risk of BBB disruption and MS. Similarly cigarette smoking, aging, vitamin D deficiency and several other compliance modulating factors will increase MS risk. To me these predicted hyertensive/compliance effects seem to correlate well with the measured observables in MS.

Trev. Tucker

For what it's worth, migraines were frequent (weekly) early in my MS. Since becoming SPMS a couple years ago they're almost non-existent. De-hydration will trigger.

PN