DrSclafani answers some questions

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby cheerleader » Fri Nov 05, 2010 2:37 pm

Sorry, Dr. S....don't mean to blab on your thread, but this hypoperfusion issue is near and dear to me....

marcstck wrote: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.


Actually, not true, Marc. A reduction in bloodflow, hypoperfusion and low O2 could create demylinating lesions. No need for reflux. People who suffer from diffuse cerebral hypoxia due to low O2 can have demyelination in the brain. It's called delayed cerebral hypoxic demyelination--happens to mountain climbers, divers, folks poisoned by CO2. This is why I continue to urge the doctors to test O2 levels pre and post angioplasty, and why Dr. Haacke is doing just that. I believe Jeff falls into the category of pwMS who had low cerebral O2 levels due to hypoperfusion and CCSVI. He came home from a week at high altitude and soon had an MS diagnosis and seven enhancing lesions. Granted, this is not everyone.

http://neuro.psychiatryonline.org/cgi/c ... l/20/4/473

Hypoperfusion and white matter lesions in rats-
http://www.ncbi.nlm.nih.gov/pubmed/11743996

Multiple sclerosis (MS) is a disease of the central nervous system characterized by patchy areas of demyelination, inflammation, axonal loss and gliosis, and a diffuse axonal degeneration throughout the so-called normal-appearing white matter (NAWM). A number of recent studies using perfusion magnetic resonance imaging in both relapsing and progressive forms of MS have shown a decreased perfusion of the NAWM, which does not appear to be secondary to axonal loss. The reduced perfusion of the NAWM in MS might be caused by a widespread astrocyte dysfunction, possibly related to a deficiency in astrocytic beta(2)-adrenergic receptors and a reduced formation of cAMP, resulting in a reduced uptake of K+ at the nodes of Ranvier and a reduced release of K+ in the perivascular spaces. Pathologic and imaging studies suggest that ischemic changes might be involved in the development of a subtype of focal demyelinating lesions (type III lesions), and there appears to exist a relationship between decreased white matter perfusion and cognitive dysfunction in patients with MS

link

There are many, many discussions on this slowed blood flow detected in MS brains, called hypoperfusion, fogdweller--this has been a very important part of the puzzle--
Here's a good one:
http://www.thisisms.com/ftopict-7708-hypoperfusion.html
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby North52 » Fri Nov 05, 2010 2:50 pm

marcstck wrote: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.


Dear Marc,

You suggest that "reflux is a key component to the CCSVI hypothesis, in that it explains the breakdown in the blood brain barrier" I really cannot see how reflux can logically break down the blood brain barrier. Reflux is seen in the larger veins using doppper ultrasound. The blood brain barrier, however, is present at the level of much smaller vessels, the capillaries and venules. I have never seen any evidence that reflux occurs at this level and would have a hard time imagining that it would.

There is good evidence that there this hypoperfusion or reduced blood flow in MS brains. You suggest that a simple reduction in blood flow cannot explain the inflammatory reaction that ensues. I would disagree with you here. I would like to propose a mechanism by which this can happen. Slow blood flow results in ischemia and activation of the coagualation cascade with production of fibrin. It is the ischemia and fibrin production that results in the breakdown of the blood brain barrier, compromise of CNS tissue and infilitration of T-lymphocytes. There is good supporting evidence for this type of hypothesis. For a more detailed description of this and supporting evidence for this hypothesis, I will refer you to my next posting "Microvascular Hypercoagulability Model for MS" The first 8 point of this hypothesis are key. What follows is somewhat technical. I also came across a paper that summarizes this process very well: http://www.ncbi.nlm.nih.gov/pubmed/18045138

North
Last edited by North52 on Wed Nov 17, 2010 7:14 am, edited 1 time in total.
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Postby marcstck » Fri Nov 05, 2010 2:51 pm

cheerleader wrote:Sorry, Dr. S....don't mean to blab on your thread, but this hypoperfusion issue is near and dear to me....

marcstck wrote: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.


Actually, not true, Marc. A reduction in bloodflow, hypoperfusion and low O2 could create demylinating lesions. No need for reflux. People who suffer from diffuse cerebral hypoxia due to low O2 can have demyelination in the brain. It's called delayed cerebral hypoxic demyelination--happens to mountain climbers, divers, folks poisoned by CO2. This is why I continue to urge the doctors to test O2 levels pre and post angioplasty, and why Dr. Haacke is doing just that. I believe Jeff falls into the category of pwMS who had low cerebral O2 levels due to hypoperfusion and CCSVI. He came home from a week at high altitude and soon had an MS diagnosis and seven enhancing lesions. Granted, this is not everyone.

http://neuro.psychiatryonline.org/cgi/c ... l/20/4/473

Hypoperfusion and white matter lesions in rats-
http://www.ncbi.nlm.nih.gov/pubmed/11743996

Multiple sclerosis (MS) is a disease of the central nervous system characterized by patchy areas of demyelination, inflammation, axonal loss and gliosis, and a diffuse axonal degeneration throughout the so-called normal-appearing white matter (NAWM). A number of recent studies using perfusion magnetic resonance imaging in both relapsing and progressive forms of MS have shown a decreased perfusion of the NAWM, which does not appear to be secondary to axonal loss. The reduced perfusion of the NAWM in MS might be caused by a widespread astrocyte dysfunction, possibly related to a deficiency in astrocytic beta(2)-adrenergic receptors and a reduced formation of cAMP, resulting in a reduced uptake of K+ at the nodes of Ranvier and a reduced release of K+ in the perivascular spaces. Pathologic and imaging studies suggest that ischemic changes might be involved in the development of a subtype of focal demyelinating lesions (type III lesions), and there appears to exist a relationship between decreased white matter perfusion and cognitive dysfunction in patients with MS

link

There are many, many discussions on this slowed blood flow detected in MS brains, called hypoperfusion, fogdweller--this has been a very important part of the puzzle--
Here's a good one:
http://www.thisisms.com/ftopict-7708-hypoperfusion.html


thanks for that, cheer. As I said, I've no doubt that hypoperfusion can cause damage to the CNS, but the papers you cite do not explain the infiltration of immune cells through the BBB. If CCSVI is THE cause of MS, the breakdown of the BBB must be explained by the hypothesis.

My particular case could be the poster child for the fact that hypoperfusion can cause CNS damage, but not immune penetration of the CNS. I definitely have a blockage in my RIJV, caused by a muscle bundle pinching it significantly. My "atypical" presentation of MS is atypical precisely because I've never shown any sign of immune system infiltration into my CNS. No O-bands, no inflammatory lesions, just one big honking lesion that doesn't enhance at the base of my brainstem.

It's for these reasons that my CCSVI dubious neurologist is willing to entertain the notion that my blocked RIJV may indeed play a big part in the pathogenesis of my disease. These very same reasons are cited by the NIH in a determination that I very likely do not suffer from MS.
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Postby Cece » Fri Nov 05, 2010 2:59 pm

marcstck wrote:thanks for that, cheer. As I said, I've no doubt that hypoperfusion can cause damage to the CNS, but the papers you cite do not explain the infiltration of immune cells through the BBB. If CCSVI is THE cause of MS, the breakdown of the BBB must be explained by the hypothesis.


How about:
The multiple sclerosis lesion: initiated by a localized hypoperfusion in a central nervous system where mechanisms allowing leukocyte infiltration are readily upregulated?

B.H.J. Juurlink


Received 4 April 1997; accepted 14 May 1997.

Abstract
A mechanism is proposed that may explain the factors that initiate a multiple sclerosis (MS) lesion. It is based upon the following two hypotheses: (i) there is a lower stimulus threshold for upregulating the mechanisms that result in leukocyte infiltration in individuals predisposed to developing MS; (ii) the MS lesion is initiated as a reduction in blood flow to a localized region of white matter. This reduction in blood flow leads to: (a) degenerative white matter changes affecting oligodendrocytes; (b) upregulation of chemokines in the endothelial cells and/or glial cells; and (c) upregulation of cell adhesion molecules on endothelial cells. Signals from the hypoxemic and hypoglycemic glial cells, likely involving myelin molecules and cytokines, result in an inflammatory immune response that results in rampant demyelination. Evidence supporting the proposed mechanism is presented, as well as suggestions on how to test the validity of the proposal.


http://www.medical-hypotheses.com/artic ... 4/abstract

It's the adhesion molecules.
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Postby marcstck » Fri Nov 05, 2010 2:59 pm

North52 wrote:
marcstck wrote: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.


Dear Marc,

You suggest that "reflux is a key component to the CCSVI hypothesis, in that it explains the breakdown in the blood brain barrier" I really cannot see how reflux can logically break down the blood brain barrier. Reflux is seen in the larger veins using doppper ultrasound. The blood brain barrier, however, is present at the level of much smaller vessels, the capillaries and venules. I have never seen any evidence that reflux occurs at this level and would have a hard time imagining that it would.

There is good evidence that there this hypoperfusion or reduced blood flow in MS brains. You suggest that a simple reduction in blood flow cannot explain the inflammatory reaction that ensues. I would disagree with you here. I would like to propose a mechanism by which this can happen. Slow blood flow results in ischemia and activation of the coagualation cascade with production of fibrin. It is the ischemia and fibrin production that results in the breakdown of the blood brain barrier, compromise of CNS tissue and infilitration of T-lymphocytes. There is good supporting evidence for this type of hypothesis. For a more detailed description of this and supporting evidence for this hypothesis, I will refer you to my next posting "Microvascular Hypercoagulability Model for MS" The first 8 point of this hypothesis are key. What follows is somewhat technical. I also came across a paper that summarizes this process very well: http://www.ncbi.nlm.nih.gov/pubmed/18045138

North


Thanks, North, that's a very interesting hypothesis that appears to have a very substantial basis in fact.

However, much of the discussions surrounding CCSVI have included the notion that the reversal of blood flow through the major vessels does indeed contribute to a breakdown of the BBB. Many pages of discussion on this very forum were spent on this issue in the months before CCSVI hit the mainstream.

If indeed hypoperfusion does result in the breakdown of the BBB, why would the inflammation seen in the relapsing remitting stages of the disease subside after a number of years, as is seen when the disease enters its SPMS phase? Logic would seem to dictate that the continued effects of hypoperfusion would lead to an increase in inflammation, rather than the eventual elimination of it.

As I have stated numerous times before, I do believe that CCSVI plays a significant role in the MS disease process, but I do find certain deficiencies in the hypothesis that lead me to question the idea that CCSVI is a primary cause of what we call MS.
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Postby marcstck » Fri Nov 05, 2010 3:00 pm

Cece wrote:
marcstck wrote:thanks for that, cheer. As I said, I've no doubt that hypoperfusion can cause damage to the CNS, but the papers you cite do not explain the infiltration of immune cells through the BBB. If CCSVI is THE cause of MS, the breakdown of the BBB must be explained by the hypothesis.


How about:
The multiple sclerosis lesion: initiated by a localized hypoperfusion in a central nervous system where mechanisms allowing leukocyte infiltration are readily upregulated?

B.H.J. Juurlink


Received 4 April 1997; accepted 14 May 1997.

Abstract
A mechanism is proposed that may explain the factors that initiate a multiple sclerosis (MS) lesion. It is based upon the following two hypotheses: (i) there is a lower stimulus threshold for upregulating the mechanisms that result in leukocyte infiltration in individuals predisposed to developing MS; (ii) the MS lesion is initiated as a reduction in blood flow to a localized region of white matter. This reduction in blood flow leads to: (a) degenerative white matter changes affecting oligodendrocytes; (b) upregulation of chemokines in the endothelial cells and/or glial cells; and (c) upregulation of cell adhesion molecules on endothelial cells. Signals from the hypoxemic and hypoglycemic glial cells, likely involving myelin molecules and cytokines, result in an inflammatory immune response that results in rampant demyelination. Evidence supporting the proposed mechanism is presented, as well as suggestions on how to test the validity of the proposal.


http://www.medical-hypotheses.com/artic ... 4/abstract

It's the adhesion molecules.


very interesting, thanks for that…
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Postby NZer1 » Fri Nov 05, 2010 6:05 pm

editing
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Stent Fracture

Postby NHE » Fri Nov 05, 2010 11:12 pm

Dr. Sclafani,
I recently ran across the following pdf PowerPoint presentation that discusses the incidence of stent fracture in the superficial femoral artery (SFA).

Stent Fractures in the SFA - Scheinert.pdf

I know that you are personally against the use of stents in the jugular veins of MS patients. I also know that several doctors are currently using stents and that many patients that have been treated for CCSVI have received stents. Some of these patients have had complications with in-stent stenosis either due to intimal hyperplasia or due to thrombosis. However, one thing that I haven't seen addressed is the expected lifetime of such stents in the jugular vein. The presentation discusses several types of stresses which could lead to fracture and some of these stresses might be found in the jugular vein. For example, axial compression of the stent might occur when one raises or lowers their head in a nodding motion and torsional strain on the stent might occur when one turns their head to look to the side. I realize that many of the stents that have been used in the jugular veins are shorter than the ones discussed for the SFA, however, the presentation still reports a fracture rate of 13.2% for stents shorter than 8 cm. My question is should patients be concerned about stent fracture in stents used for jugular veins? It is still very early in the history of stent use in jugular veins, but could such failures become more common in the not too distant future? Is the possiblity of stent fracture a reason to avoid stents in the jugular veins? The patency rate of Nitinol Smart stents reported in the presentation at only 60% after just 1 year is not very encouraging. Moreover, the patency rate of fractured stents after 20 months is also disturbingly low (around 10%).

Thanks in advance for your response, NHE
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Postby drsclafani » Sat Nov 06, 2010 7:53 am

marcstck wrote:Hi Dr. Sclafani,

As my "atypical" case illustrates (a muscle bundle external to the vein pinching it quite significantly, but apparently causing no blood flow turbulence) , not every stenosis or blockage results in blood flow reflux, which is actually at the heart of the CCSVI hypothesis.
]

Marc, while it is acceptable for you to discuss publicly your condition, It is not acceptable for me to do so (which i would love to do) without your explicit permission. It would be a HIPPA violation. So, let me know and we can discuss your blockages on this site. Let's just say that i disagree with your synopsis of your condition and leave it at that for the moment. At the very least, you and I have to have another review of your case to clarify some issues. We can do that in person or on line privately if you wish

Venous stenosis is merely the agent that causes this reflux, so the stenosis itself, absent blood flow reflux, is hypothetically not the problem.

in other words you are saying cause without effect is not important. Sort of like the tree falling in a forest with no one to hear it fall. Theoretically I can agree with that. HOwever, if we are finding outflow obstructions (i would rather use this all encompassing term rather than stenosis) predominantly in symptomatic patients, I would consider it a problem leading to another problem.

Since this is the case, isn't the aggressive seeking out of any stenosis (such as Dr. Sinan's method of slightly inflating the azygos looking for any signs of stenosis) and then treating it overkill? Shouldn't blood flow disruption and reflux, rather than simply the presence of stenosis, be the arbiter of whether or not to treat?


I lost your logic there. Dr Sinan is not dilating obstructed veins in patients without symptoms...thus an indication to treat outflow obstructions is symptomatic patients. Moreover, i believe that Dr Sinan is testing for CCSVI by ultrasound, is he not? Does that not indicate that he is looking for outflow obstructions in patients who DO have evidence of reflux. So I would not think that looking for outflow obstructions by "compliant balloon inflation" is overkill. Remember these malformations are not easily visible on venography because the septations might isolate areas of the vein from the contrast media column.

It seems to me that many IR's are ballooning and even stenting just about any sign of stenosis they come across during a catheter venogram. I understand that blood flow problems are detected when the dye is injected into the vein, but, at least from some patient accounts, this doesn't seem to be the criteria being used to determine whether or not to treat.

All over the Internet, it seems that the CCSVI argument has gone stenosis happy, concentrating on narrowed veins rather than the impact that they have on blood flow, which in some cases is actually negligible.

Marc, the statement, that some of these stenoses have negligible impact on blood flow, is unfounded. While it might be true, the statement is not based upon fact.

I think we have to take these internet accounts with a grain of salt. We are unclear from these accounts what stenoses were present, what the logic was for the IR to do the angioplasty, what flow looked like on the live fluoroscopy images, and many more considerations .

To my medically untrained mind, it would seem that a stenosis would need to be rather severe to cause blood to actually reverse course in the vein.

I wish i could tell you what degree of narrowing results in significant blood flow disturbance, but i cannot yet. In many circumstances, that narrowing is rather dynamic actually. Veins are highly compliant, in essence that have great capacities to distend or collapse depending upon blood flow. When the vein is less compliant, as happens in CCSVI, the capacity to distend may be reduced. Also if there is an outflow obstruction, blood flow is diverted to paths of less resistance, so the normal parts of the vein might not distend as much. So the % of narrowing (diameter or area the narrowed segment divided by the diameter or area of the normal vein) might be a gross underestimation.

Furthermore, the veins are low pressure systems. while 70% stenosis is considered significant in an artery, smaller percentages of narrowing are significant in veins because the pressure driving blood across the narrowing is so much lower.

In my case, the narrowing of the vein is quite severe, yet Dr. Zamboni thinks no treatment is necessary. But we consistently hear of blockages of 50% and sometimes less, being treated. Is this being overaggressive?


Marc, that muscle is something that is a special case. I dont want to speak about it here, without your permission.

I am inclined to treat stenoses in the 30% range, but this might not be aggressive enough. of course other factors, such as turbulence, collaterals,symptoms, progression of disease, etc will factor into that decision.

Am I way off the mark here?


you are never off the marc
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Postby North52 » Sat Nov 06, 2010 8:14 am

marcstck wrote:
North52 wrote:
marcstck wrote:If indeed hypoperfusion does result in the breakdown of the BBB, why would the inflammation seen in the relapsing remitting stages of the disease subside after a number of years, as is seen when the disease enters its SPMS phase? Logic would seem to dictate that the continued effects of hypoperfusion would lead to an increase in inflammation, rather than the eventual elimination of it.



Dear Marc,

I will take stab at this. Is there really less inflammation in the SPMS phase? In SPMS patients with continued progressive worsening, I would suspect continued hypoperfusion and inflammation. Some patients do plateau, however. In these patients, I suspect inflammation may have subsided as all the tissue that could be destroyed has been destroyed. Why have inflammation if there is no more viable tissue? The underlying hypoperfusion would still, however, be present.

North
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Postby pklittle » Sat Nov 06, 2010 8:54 am

drsclafani wrote:
pklittle wrote:
drsclafani wrote:
pklittle wrote:
pklittle wrote:Dr. Sclafani,
Since each Dr. treating CCSVI seems to have their own twist (no pun) on how to test, pick the balloon size, etc, what advice would you give a patient that has been treated with venoplasty but had no relief of symptoms? More specifically, would it be worthwhile to seek treatment elsewhere by someone who is also experienced but who's approach is a bit different?
Pklittle


Bringing this over from the bottom of the previous page in hope Dr. S will see it. Thx


i think that the next step is to determine whether there is or is not improvement in the Doppler results. If the Doppler is the same, i think another opinion is valuable. if the doppler shows eradication of the ccsvi criteria, then perhaps the brain damage is too great. but of course this decision is between patient and doctor


Dr. Sclafani, thanks for your reply. I am going to have an ultrasound tomorrow! I am embarrassed to ask... are all ultrasounds Doppler?
I am glad to be having the test, but I am concerned because:
1) I don't know if the technician knows squat about CCSVI and how to check for it. I am having the test locally.
2) The local doctor to receive the results does not have a prior Doppler to compare it to.. so who's to say if it is the "same" as anything before or after angioplasty I had in June?


this is an extremely good point. i would not just get an ultrasound. it would be an ultrasound with color doppler and it must be done by someone who has experience and understanding of the zamboni techniques; i go on record that treating patients without setting up the methodology of using doppler ultrasound after the procedure needs to be addressed. Once could argue that one should not undergo this treatment unless one has attained connection with the ultrasound lab willing to provide the zamboni technique of ultrasound.

IT IS AN AREA THAT YOU NEED TO HAVE SOME ACTIVISM ABOUT. YOU, THE CONSUMERS, WOULD NEVER BUY AN ELECTRIC CAR IF YOU DIDNT KNOW THERE WAS A PLACE WHERE YOU COULD CHARGE THE BATTERIES.

WORK LOCALLY TO ASSURE THAT YOU HAVE A CENTER THAT WILL DO THAT. USE YOUR POCKETBOOKS AND WALLETS TO VOTE FOR ONE OR TWO LABS THAT WILL PROVIDE WHAT YOU NEED

okay, i can get off my soap box now

i know you are in a hurry, but


ok, now I know for certain I have not only restenosed but my vein is a lot worse. I am pm'ing you Dr.

Just a note to point out to those reading that even if you are treated and see no symptomatic benefits, you STILL should have followup because your vein(s) may protest by getting worse, and ms symptoms can become worse.
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Postby drsclafani » Sat Nov 06, 2010 8:58 am

NZer1 wrote:Hi Marc I am in agreement with you on this. Although people have malformations and stenosis it is the reflux that causes the issues, and it is over time that the severity creates the 'disease'.
we must understand that the reflux may not be linear in its effects. For example, certain times of high blood flow will stress the system more.


Dr S your reply to my question probably doesn't cover the spectrum of symptoms that PwMS have and other diseases that are being linked to these blood flow issues. There seems to be more grey areas to consider, for instance the azygous issues and the 50 plus subgroups of CCSVI that Dr Haacke speaks of.

NZer1, i am unclear what you mean about the grayness of the azygos issue. The azygos vein drains the spinal cord and acts as a secondary channel to drain the brain when other veins are malformed. it is an important vein in this issue, not more important, just important. Finding these outflow obstructions in the azygos vein is more challenging for technical reasons, not because azygos involvement is unclear.

Indulge my interpretation of haacke. I believe he is noting that there are many variations in how the outflow obstruction looks, not about the ccsvi clinical presentations.
I think that once the collaterals have established and taken the flow away the redirection and size challenges the flow and causes the reflux.

These collaterals do not typically have valves, so their direction and rate of flow is highly variable. This is not a problem when their size is small and their flow is not great. However, it is theoretically possible that the flow in the collateral might reverse and actually increase reflux in certain conditions.

If the collateral was stream lined for flow of low pressure/gravity flows the reflux probably wouldn't happen.


this is not true. Some of the collateral circuits require that the venous blood go away from the heart before it can return to the heart. it is this collateral flow that may result in intracranial venous injury.


If the one way valve was high up in the return flow system it would cater for all and any stenosis in the system.


if the one way valve were higher, the problem would be worse if the valve was malformed. it would mean that there would be less collateral veins in the neck to relieve some of the back up of blood and more blood would be forced back through collaterals in the brain.

It seems the valves were there for a good reason in the first place to only improve flow will not stop reflux, which will occur to some degree in normal life, caused by movement of the neck as one example.

The purpose of those valves, for those readers who are unclear, is to prevent flow from the heart from backing up into the jugulars and then into the brain. The valves also encourage flow in the direction toward the heart. Since these valves are absent normally in about 15% of unaffected humans, reflux from heart back into the jugulars does not commonly cause problems because the refluxed blood likely travels up to the dural sinuses and then returns to the heart. There are reports of serious problems, such as transient global amnesia that occurs from this type of reflux.

REMEMBER THERE ARE TWO TYPES OF REFLUX,
ONE WHERE BLOOD FLOWS BACK FROM THE HEART AND UP THE JUGULAR VEIN
AND
ONE FROM THE BRAIN, DOWN TO THE VALVE AND BACK UP TO FIND AN ALTERNATE PATHWAY OUT.

We have to keep them straight when we talk about reflux.

The symptoms from reflux seem to me to be the same as MS symptoms and the symptoms that are found in diseases involving blood flow issues from the brain of patients that haven't been dx'ed as PwMS are the same.

i am of the opinion that some of the symptoms in patients with MS may be symptoms of CCSVI and other symptoms might be related to demyelinzation and other brain damage. The two entities might actually coexist.


Dr S why would the valves be in the veins draining the brain?

i think i answered this above.
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Postby drsclafani » Sat Nov 06, 2010 9:03 am

buggs wrote:I am sorry in advance for my ignorance, I was wondering where is Dr. Sclafani from? Do you do procedures and are you able to give me some advice??
dr sclafani is from new york city
whether i do procedures is a complicated question. I am happy to answer this in a private message.

I have a Dopplar Ultrasound that says my LIJ does not close upon me sitting up. What does that mean every one elses seems to be stuck closed???


it is difficult to interpret such reports. sometimes the doppler ultrasound is done and interpreted incorrectly for ccsvi. other times the report is interpreted incorrectly by patients.

write your report accurately on here and we can have a look at it together, if you would like
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drsclafani
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Postby drsclafani » Sat Nov 06, 2010 9:05 am

Cece wrote:Off the marc?

drsclafani wrote:I do not think that reflux up the jugular vein is really the pathophysiology of this entity. Dr. Zamboni suggests that it the obstruction that is the real problem. This leading to reversal of flow through small vessels not designed to take that kind of flow. I do not think the problem is pressure or reverse pressure. it is flow

http://www.thisisms.com/ftopicp-98309.html#98309

Not sure I understand that, but it seemed relevant. Does a vein pinched by a muscle still grow collaterals?


marc
you have the entire world of ms now wondering about your condition.
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Postby drsclafani » Sat Nov 06, 2010 9:05 am

spiff1970 wrote:Hi,

Does anyone have any information about the rate of thrombosis following the placement of stents in the jugulars? I heard that there has been many cases but I've only seen a couple of them reported here. More evidence, please.

best,

Spiff


yes, we need more evidence
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