Chronic Cerebrospinal Venous Insufficiency (CCSVI)-

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

Postby mrhodes40 » Mon Mar 09, 2009 6:49 pm

metal fatigue

That is a very good point.

The only thing I can think of is that the muscles supporting the venous structure are not receiving the proper stimulation from nerves (due to MS), and therefore the relaxed support causes some alteration in flows;.


There is a thing called neurogenic vasodilation but that affects arteries not veins which are largely passive. Speaking of which why these few veins? why not arteries? if it were a muscular thing that would be more credible.

No matter what the big bottom line is that this area needs a lot of reseach and clarification.

I will be asking my people a lot of questions and will benefit greatly by the fact you went fist and I have had a long time to think about it and come up with some questions for them. I'm bothered by why you had only one, what does that mean? does it mean a lot or a little to them if that happens to me? And what about my dopplers, I'll gladly sign up for the venography, no problem if they offer it. I've run through that mentally too.

My fear though is that they won't see anything much at all and I will end up waiting for Zamboni to come out with more information.

Thanks Cure for sharing everything so freely.
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Postby CureOrBust » Mon Mar 09, 2009 7:03 pm

mrhodes40 wrote:I'm bothered by why you had only one, what does that mean? does it mean a lot or a little to them if that happens to me?
I know my neurologist lost interest very quickly when he only found one, and did not duplicate the results as Zamboni presents them. Personally, I am a little concerned that I have a reflux in a major valve between my brain and heart. 8O

mrhodes40 wrote:And what about my dopplers, I'll gladly sign up for the venography, no problem if they offer it. I've run through that mentally too.
brave woman :!:
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Postby sou » Mon Mar 09, 2009 7:03 pm

Hi.

The only thing I can think of is that the muscles supporting the venous structure are not receiving the proper stimulation from nerves (due to MS), and therefore the relaxed support causes some alteration in flows;.


The muscles around blood vessels are smooth muscles. The smooth muscles of the endothelium are not controlled by the nervous system but react to hormonal stimuli by neighbor cells.

sou
Shortest joke: "We may not be able to cure MS but we can manage its symptoms."
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Cure.

Postby AndrewKFletcher » Tue Mar 10, 2009 12:41 am

There is another possibility you might be overlooking.

You are using Inclined Bed Therapy if I am correct?

This being the case, a reversal of the internal varicose veins would be expected within 4 weeks or more, but possibly within fewer weeks.

Could IBT have began to work on the pressures inside the venous return? I believe this is a definite rather than a possibility.

You may want to inform Professor Zamboni about this as failing to do so might skew his results.

But more to the point it might help people avoid unnecessary surgery in the majority of cases.

Varicose veins in the legs go flat in 4 weeks, Obviously larger vaicose veins will take longer to return to normal vein size. This should tell us all something about how the veins bulge in the first place considering all we have done is avoided sleeping flat.

High blood pressure quickly falls when IBT is used, another consideration for Professor Zamboni and his team.

Still not had a reply from him yet, but I am sure he has read about my research as I am not the only person to have contacted him about it.

Andrew
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Postby gibbledygook » Tue Mar 10, 2009 6:35 am

In the paper by Ruiz, Gaillaud et al "Craniocervical Venous System in relation to cerebral venous drainage" posted by Marie on page 24 of this thread I noticed that the discussion centers quite a lot on the different venous drainage going on when supine and upright. If I remember rightly, the outflow from the internal jugular vein is negligible when in the upright position. Maybe this is why IBT helps with cerebral MS since the reflux from the internal jugular is avoided since drainage occurs from other veins.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby mrhodes40 » Tue Mar 10, 2009 12:36 pm

It does Gibbles, here's the abstract
from here
http://www.ajnr.org/cgi/content/figsonly/23/9/1500

BACKGROUND AND PURPOSE: Passing from the supine to the upright position favors cerebral venous outflow into vertebral venous systems rather than into the internal jugular veins. We sought to determine venous connections between dural venous sinuses of the posterior cranial fossa and craniocervical vertebral venous systems.

METHODS: Corrosion casts of the cranial and cervical venous system were obtained from 12 fresh human cadavers, and anatomic confirmation was made by dissection of three previously injected fresh human specimens. MR venography was performed to provide radiologic correlation.

RESULTS: The lateral, posterior, and anterior condylar veins and the mastoid and occipital emissary veins were found to represent the venous connections between the dural venous sinuses of the posterior cranial fossa and the vertebral venous systems. This study revealed the nearly constant presence of the anterior condylar confluent (ACC) located on the external orifice of the canal of the hypoglossal nerve. The ACC offered multiple connections with the dural venous sinuses of the posterior cranial fossa, the internal jugular vein, and the vertebral venous system. All these structures were shown by MR venography.

CONCLUSION: The lateral, posterior, and anterior condylar veins and the mastoid and occipital emissary veins connect the dural venous sinuses of the posterior cranial fossa with the vertebral venous systems. These connections are clinically relevant, because encephalic drainage occurs preferentially through the vertebral venous system in the upright position. The ACC is a constant anatomic structure that may play an important role in the redirection of cerebral blood in the craniocervical region.

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Postby cheerleader » Tue Mar 10, 2009 1:11 pm

Cure:
He did do venographies in the first study. This is how he was able to find the stenoses. Stenoses are only implied in the TCD tests by reflux and anomalous blood flow...
Finally, in 37% of cases B-mode high-resolution imaging permitted
to detect directly closed stenosies in the IJVs (Fig 1a, 1b), (Tab II).

Only 37% showed stenoses thru the non-invasive test, but 100% had them as shown thru venography
Here are the results again:

SELECTIVE VENOGRAPHY
Sixty-five subjects with MS fulfilling the ECD-TCCS screening criteria and 48 controls of the HAV-C group, underwent selective catheterism of the azygous and IJV system via the transfemoral route. Venography was performed being aware of patients’ diagnoses. We considered a significant stenosis to be any venous lumen reduction greater than 50%.24-28 In addition, selective venography allowed us to measure with a manometer the pressure expressed in cm/H2O in the superior vena cava, in the azygous vein, and in both the IJVs.

]Selective venography enabled us to localize exactly not only the places of venous steno-obstruction, but also, by comparing the flow direction data collected by the ECD-TCCS method, to identify the pathways of venous reflux and substitute collateral circles. In this way it was possible to delineate a picture of chronic cerebrospinal venous insufficiency (CCSVI) associated to MS, for which we found four principal patterns, as shown in Fig. 3.

Figure 3: Patterns of CCSVI observed in MS cases

Fig.3:
Normal) Exemplification of normal extracranial venous outflow direction. In particular, the black arrows depict the drainage of the IJV system into the SVC, and of the vertebral plexus (Vplex) outward from the spinal cord into the azygous system (AZY).

• Type A (30%): This pattern is characterized by a steno-obstruction of the proximal azygous, associated with a closed stenosis of one of the two IJVs (red crosses). Reflux is always present, under all postural conditions, in the stenosed IJV (red arrow), with a compensatory controlateral IJV that appears with an ample CSA. Reflux in the DCVs was detected by the
means of TCCS in 60% of cases. In the azygous vein the reflux has an
effect as far as the lumbar veins, being able to re-enter the caval circle
either through the system of the hemiazygous vein- left renal vein, or by
rising again inside the rachis.

• Type B (38%): This pattern is characterized by significant stenoses of both IJVs and the proximal azygous (red crosses). Reflux is present in all three venous segments (red arrows). Cerebral venous outflow for overcoming the IJVs stenosis re-enters the heart mainly through cervical collateral circles (Fig. 1b); for the hampered azygous vein outflow, the collateral circles include again the intra-rachidian pathway (Fig.3), or the system of the renal-hemiazygous.

• Type C (14%): This pattern is characterized by bilateral stenosis in both
IJVs, with a normal azygous system (red crosses). Reflux (red arrows)
occurs in the IJVs but not in the VVs, with cervical or intracranial collateral
circles that shunt blood towards the superior vena cava or the azygous
vein system, respectively. The resulting overload of the azygous system is depicted by black bold arrows.

• Type D (18%): In this pattern the azygous system was constantly affected in various segments (red crosses), resulting in a forced venous drainage towards the intrarachidian circles in an upward direction (red arrows)
(Fig.3). The vertebral veins appeared to be refluent, and the intracranial
collateral circles seek to gain the IJVs, as confirmed by reflux detection in
DCVs in 90% of cases. At times, the IJVs were also affected (6 cases,
50%), causing an additional obstruction in these patients.



cheerleader wrote:The docs didn't see anything blocking your jugular flow, right? They claim it was the valve?
Nope, nothing but the jugular valve failed the 5 tests he has presented in his paper. I did NOT do the invasive tests. 8O


I hate to say it, Cure and Marie, but I think venography is the only way to know for sure. The doppler test shows the reflux and blood flow patterns....but the venography is what detected the stenoses in 63% of the MS patients. Since you only failed one test, I'm not sure, Cure, if you're up for this.

I'm talking to some new docs here in socal for testing, and they want us to be prepared to do the venography if any reflux is shown. I know it's invasive and a bit daunting, but I think it's the only way to know for sure.

AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby gibbledygook » Wed Mar 11, 2009 2:57 am

How about ridding ourselves of stenoses with a bit of mild ultrasound!!!

1: Ultrasound Med Biol. 2007 May;33(5):663-71. Epub 2007 Mar 26. Links
Mechanisms by which low-intensity ultrasound improve tolerance to ischemia-reperfusion injury.Bertuglia S.
CNR Institute of Clinical Physiology, Faculty of Medicine, University of Pisa, Pisa, Italy. sibert@ifc.cnr.it

Recent studies show that low-intensity ultrasound (US) increases endothelial nitric oxide (NO) levels in different models both in vitro and in vivo. Ischemia-reperfusion (I/R) injury is characterized by endothelial cell dysfunction, mainly as a result of altered shear stress responses associated with vasoconstriction, reduced capillary perfusion and excessive oxidative stress. This review provides an overview of the microvascular effects of low-intensity US and suggests that US exposure can be a method to provide tolerance to I/R damage. The hamster cheek pouch, extensively used in studies of I/R-induced injury, has been characterized in terms of changes of arteriolar diameter, flow and shear stress. The low-intensity US exposure reduces vasoconstriction and leukocyte adhesion and increases capillary perfusion during postischemic reperfusion. These effects may be the result of enhanced fluctuations in shear stress exerted by the flowing blood on the vessel wall. The fluctuations in turn are due to mechanical perturbations arising from the difference in acoustical impedance between the endothelial cells and the vessel content. We believe that periodic pulses of US may also cause a sustained reduction of oxidative stress and an enhanced endothelial NO level by increasing oscillatory shear stress during postischemic reperfusion. Low-intensity US exposure may represent a safe and novel important therapeutic target for patients with acute coronary syndromes and for treatment of chronic myocardial ischemia.

PMID: 17383799 [PubMed - indexed for MEDLINE]
link

I actually possess a small, cheap, handheld ultrasound device for use on my now healed achilles tendon...If only I knew exactly where my azygous vein was blocked I could zap the area!


Here's one for Lyndacarol:

1: Endothelium. 2007 Jan-Feb;14(1):17-24. Links
Elevated glucose attenuates agonist- and flow-stimulated endothelial nitric oxide synthase activity in microvascular retinal endothelial cells.Connell P, Walshe T, Ferguson G, Gao W, O'Brien C, Cahill PA.
Vascular Health Research Centre, Faculty of Science and Health, Dublin City University, Dublin, Ireland.

Impaired vasoactive release of opposing vasodilator and vasoconstrictor mediators due to endothelial dysfunction is integral to the pathogenesis of diabetic retinopathy. The aim of this study was to determine the effect of hyperglycemia on the expression of endothelial nitric oxide synthase (eNOS) and the release of nitric oxide (NO) in bovine microvascular retinal endothelial cells (BRECs) under both static (basal and acetylcholine stimulated) and flow (laminar shear stress [10 dynes/cm2 and pulsatile flow 0.3 to 23 dynes/cm2) conditions using a laminar shear apparatus and an in vitro perfused transcapillary culture system. The activity and expression of eNOS, measured by nitrate levels and immunoblot, respectively, were determined following exposure of BRECs to varying concentrations of glucose and mannitol (0 to 25 mM). Under static conditions the expression of eNOS decreased significantly following exposure to increasing concentrations of glucose when compared to osmotic mannitol controls and was accompanied by a significant dose-dependent decrease in nitrate levels in conditioned medium. The acetylcholine stimulated increase in NO release (2.0 +/- 0.3-fold) was significantly reduced by 55% +/- 5% and 65% +/- 4.5% following exposure to 16 and 25 mM glucose, respectively, when compared to osmotic controls. In parallel studies, glucose significantly inhibited both laminar shear stress and pulsatile flow-induced activity when compared to mannitol. We conclude that hyperglycemia impairs agonist- and flow-dependent release of NO in retinal microvascular endothelial cells and may thus contribute to the vascular endothelial dysfunction and impaired autoregulation of diabetic retinopathy.

PMID: 17364893 [PubMed - indexed for MEDLINE
link
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Postby AndrewKFletcher » Wed Mar 11, 2009 4:26 am

This is one reason. Another reason is that the longer the veins remain normal size the more resistance to bulging they retain as the cells in the veins become contracted.

But there is another question that remains un-answered. IBT has been shown to repair the damaged nervous system. So we are not just looking at a method of addressing the pressures that cause the internal veins to swell but we must also be looking at what drives the circulation in the nervous system and as there is no conclusive explanation for what causes this fluid to circulate other than posture and respiration, are we looking at an effective way to arrest and reverse ms? I believe this is the case!

Will it work for everyone with ms and can it prevent ms?
We can only determine these questions by testing IBT with more people who have ms.

Is it going to be pain free? Probably not as pain usually arrives before recovery based on many reports. However, the arrival of the electric stabbing pain by the majority of people using IBT has been welcomed rather than causing them to reject this therapy.
Andrew

gibbledygook wrote:In the paper by Ruiz, Gaillaud et al "Craniocervical Venous System in relation to cerebral venous drainage" posted by Marie on page 24 of this thread I noticed that the discussion centers quite a lot on the different venous drainage going on when supine and upright. If I remember rightly, the outflow from the internal jugular vein is negligible when in the upright position. Maybe this is why IBT helps with cerebral MS since the reflux from the internal jugular is avoided since drainage occurs from other veins.
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Postby CureOrBust » Wed Mar 11, 2009 4:56 am

sou wrote:The smooth muscles of the endothelium are not controlled by the nervous system but react to hormonal stimuli by neighbour cells.
Sorry for not being clear, however, I was just thinking (wildly) about the skeletal muscles, and their effect on internal organs; on the crazy assumption that there would possibly be some connecting tissue to them, and may affect the position of something). I do not believe it to be the case, just going out on a thin limb.
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Postby CureOrBust » Wed Mar 11, 2009 5:22 am

cheerleader wrote:Cure:
He did do venographies in the first study. This is how he was able to find the stenoses. Stenoses are only implied in the TCD tests by reflux and anomalous blood flow...
Your right, I was thinking the quote came from another study. My mistake.

cheerleader wrote:Since you only failed one test, I'm not sure, Cure, if you're up for this.
If others DO duplicate the results, and/or they do a venography, then it will be more of a driver, and a possibility, maybe, after Zamboni's presentation of his "treatment", possibly, maybe. :cry:

cheerleader wrote:I'm talking to some new docs here in socal for testing, and they want us to be prepared to do the venography if any reflux is shown.
This is what I do not understand. Why are my people not concerned that i have a reflux in a major valve? :?
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Postby gibbledygook » Wed Mar 11, 2009 10:17 am

NSAIDS to inhibit build-up of vascular tissue:

1: Shi Yan Sheng Wu Xue Bao. 2003 Apr;36(2):85-90.Links
[Inhibition of vascular smooth muscle cell proliferation by non-steroidal anti-inflammatory drugs][Article in Chinese]


Wang YQ, Brooks G, Harper J, Li YQ, Zhu CB, Yuan WZ, Wu XS.
College of Life Science, Hunan Normal University, Changsha 410081.

Abnormal vascular smooth muscle cell (VSMC) proliferation is known to play an important role in the pathogenesis of atherosclerosis, restenosis and instent stenosis. Recent studies suggest that salicylates, in addition to inhibiting cyclooxygenase activity, exert an antiproliferative effect on VSMC growth both in vitro and in vivo. However, whether all non-steroidal anti-inflammatory drugs (NSAID) exert similar antiproliferative effects on VSMCs, and do so via a common mechanism of action, remains unknown. In the present study, we demonstrated that the NSAIDs, aspirin, ibuprofen and sulindac induced a dose-dependent inhibition of proliferation in rat A10 VSMCs (IC50 = 1666 mumol/L, 937 mumol/L and 520 mumol/L, respectively). These drugs did not show significant cytotoxic effects as determined by LDH release assay, even at the highest concentrations tested (aspirin, 5000 mumol/L; ibuprofen, 2500 mumol/L; and sulindac, 1000 mumol/L). Flow cytometric analyses showed that a 48 h exposure of A10 VSMCs to ibuprofen (1000 mumol/L) and sulindac (750 mumol/L) led to a significant G1 arrest (from 68.7 +/- 2.0% of cells in G1 to 76.6 +/- 2.2% and 75.8 +/- 2.2%, respectively, p < 0.05). In contrast, aspirin (2500 mumol/L) failed to induce a significant G1 arrest (68.1 +/- 5.2%). Clearer evidence of a G1 block was obtained by treatment of cells with the mitotic inhibitor, nocodazole (40 ng/ml), for the final 24 h of the experiment. Under these conditions, aspirin still failed to induce a G1 arrest (from 25.9 +/- 10.9% of cells in G1 to 19.6 +/- 2.3%) whereas ibuprofen and sulindac led to a significant accumulation of cells in G1(51.8% +/- 17.2% and 54.1% +/- 10.6%, respectively, p < 0.05). These results indicate that ibuprofen and sulindac inhibit VSMC proliferation by arresting the cell cycle in the G1 phase whereas the effect of aspirin appears to be independent of any special phase of the cell cycle. Irrespective of mechanism, our results suggest that NSAIDs might be of benefit to the treatment of vascular proliferative disorders.

PMID: 12858504 [PubMed - indexed for MEDLINE]



link
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Postby mrhodes40 » Wed Mar 11, 2009 2:34 pm

Cheer:
Yes, I agree venography is where it is at, clearly. I have not been told to prepare for possible venography so do not believe they are thinking along those lines for friday.

Cure: I understood, believe it or not, the wild muscular idea in your post, the interesting thing about this is you kind of have to go that far to find an "explanation" that isn't what Zamboni is offering. Then you are sort of wandering in the weeds: occams razor and all that.

I'm a nervous ball of energy I spend all day re reading the papers I have copies of regarding Zamboni's work, getting ready to talk and ask the "right" questions Friday.

And now more baloney slicing from the peanut gallery;

I've been read in the Zamboni papers again trying to glean more understanding and also reading some of what he used for reference. Sometimes I get a fuller understanding, for example one paper about venous issues mentions that all people with venous ulcers have other changes in their SKIN too, indicating the different veins may be different to begin with in terms of collagen....this suggests that it is not all about pressure and there is some genetic issue to begin with. For me, knowing Z used that reference clarifies a statement he made in email that his proceudre may work in tandem with other approaches--in other words we may need something to address the eventually-clarified systemic issue as well.

But along the lines of reading those references, there are a lot of mental/brain issues that show cerebral venous problems. About the 4th time you hit a paper that talks about venous drainage, you start to go hmmmm..... this is not such a new idea at all.

Read this bit from an abstract found

CLICK HERE
IN approximately 90% of human internal jugular veins (IJVs) there is a valve. 1,2 It is situated directly above the termination of the IJV in the inferior bulb, the position of which may vary slightly from being almost directly posterior to the head of the clavicle to a position 3 cm further inferior and 3 cm further lateral. 3 The valve prevents backward blood flow toward the brain when the intrathoracic pressure acutely increases and can create transvalvular gradients of up to 100 mmHg. 3 The competence of the valve has been found to be crucial for developing a transcranial blood pressure gradient during cardiopulmonary resuscitation with closed-chest compression. 4 In addition, this valve prevents sudden increases in the IJV pressure during coughing or positive pressure ventilation and may thus protect the brain from acute increases in intrathoracic pressure. 3,5


Ok so the valve is there protect the brain.

Another from CLICK HERE

Background and Purpose. Jugular venous valve insufficiency may play a role in different neurological diseases. ---snip!--


Well, fine then. We all think so.
Another one
HERE

Valvular insufficiency (either left or rightsided, or bilateral) was identified in 85% of patients with TGA,and in 45% of controls (p = 0.008).

That one used valsalva to assess for reflux, not the test Z uses so the 45% controls is not the same. But notice that the difference between so called healthy normal controls and patients with TGA is small in terms of pressure. This to me suggets the brain can't take a lot of difference here, reflux is hard on it (BTW, these TGA patients do not have abnormal white spots on MRI, I looked) But note that the TGA issue is often one of a post valsalva problem. The valsalva is the thing you do if --ahem!--constipated and you hold your breath and push..got it?

If you have TGA it appears the mechanism may be that your jugular valve is not competant and that "push" results in backflow into the brain briefly--Wham!--you get transient amnesia. It goes away, perhaps not to happen again for months.

But, accepting Z work, MSers have reflux that happens all the time not just with valsalva. Even though the times are smaller it is with every breath all the time. It is not at all hard to understand that this constant whirl and chaotic blood flow might cause an the issue we call MS esp when you realize that it is these specific veins that are attached to those specific lesion area that are affected. I mean why not arteries? If you think it is the immune system coming in and attacking why only veins? Why do lesions grow in the direction of the vein and not into the brain?

Taken together with the idea of the neuro protection of the brain by the jugular valve and apparent acceptance of the idea the brain needs protection from these chaotic pressure changes, is it at all odd that we would think this work done by Zamboni is critically important and not just some new whacky theory?

But as I schlepp along the pubmed path I keep hitting these hints that neuro issues are associated with venous issues, and that in some quarters it is pretty well accepted.

I am pleased to be part of what could be termed a grass roots effort to get this information in front of people who will listen and assess it---NOW, not a year from now, and not 5 years from now. Now.
Thanks to everyone contributing to this thread I read every word with interest............peace everyone
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Postby cheerleader » Wed Mar 11, 2009 3:11 pm

Thanks for that, Marie...I really enjoy your deep thoughts-and your nervous energy.

Why do only 90% of human beings have a jugular vein valve??? Seems like it is an important feature! There must be a genetic variant at work here. I'd love to see what the 10% of folks missing the valve had in common. In what situation would a human being not need a jugular vein valve? Is this a birth defect, like a cleft palette or club foot?

Venous backflow is very serious. Transient global amnesia is a serious but temporary condition. It is caused by limited venous reflux. Imagine that the reflux does not stop...

MS shows up in young adults. Could it be that a childhood with congenital venous reflux eventually builds up damage in the brain and spine, until it can no longer be hidden? That's when we diagnose MS. The MS patient relapses and remits- the brain is able to heal and recover for awhile. Inflammation can be tamped down, the brain can rewire. But time and venous damage march on. Until finally the damage can no longer be overcome and the MS is deemed progressive. And then medicine just looks the other way.

Thanks for keeping this discussion on the front burner, right now, Marie. We all benefit from your research and thoughts.

Cure, I don't know why your docs aren't more concerned with your jugular reflux. I really think you need to ask them. How would they treat this if you were not diagnosed with MS?
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby cheerleader » Thu Mar 12, 2009 7:51 am

Received a PM from a doctor who has been following this thread with great interest- because their dept. is still in the process of writing up the study, they wish to remain anonymous. But they wanted to share, and offer encouragement. English is not their first language....

I think this information would be important for you and other ThisIsMS participants. We have just started the study to confirm ultrasound results got by Zamboni, the first group (5 patients) of MS patients was assessed.
I should say that datailed ultrasound examination according to Zamboni's protocol is not an easy issue (although we are skilled in venous ultrasound examination of lower extremities), and we are sure that we have overlooked many important things. Undoubtedly, more training of this unusual exam is needed.
Anyway, ALL FIVE patients were found pathologic changes in their veins draining the brain. The next group of patients is scheduled in the beginning of April.


AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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