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It's now been over 18 months since the news of Dr. Zamboni's vascular theory of MS, the CCSVI hypothesis, first made its way into the consciousness of the greater Multiple Sclerosis patient population. Touched off by news reports on Canadian television channel CTV, an inferno of hope raced through MS patients worldwide, and a firestorm of controversy regarding almost every aspect of the hypothesis was ignited, a conflagration that seems to only burn more intensely with each passing week. The relatively simple CCSVI hypothesis (which postulates that blockages in the veins draining the central nervous system lead to or contribute to the MS disease process) has managed to pit physician against physician, physician against patient, and patient against patient. While the various factions duke it out, an estimated 15,000-20,000 MS sufferers have undergone CCSVI venoplasty, with a wide variety of resulting outcomes, ranging from dramatic benefit to no benefit whatsoever to, in rare cases, a worsening of disease symptoms.
Several key questions have emerged regarding CCSVI during the last year and a half, primary among them whether or not CCSVI and MS have any link whatsoever, and if so, whether the venous anomalies collectively known as CCSVI are the cause or an effect of the disease. We've seen a steadily increasing flow of CCSVI research results, providing enough conflicting data to fuel all sides of the argument. As with all things Multiple Sclerosis, CCSVI presents a complex picture, and despite evangelical believers/nonbelievers on all sides of the squabble, at present the ultimate outcome of the CCSVI conundrum is as clear as mud. Here then is a brief look at some of the issues currently being batted about, with some small attempt on my part to make some sense of it all.
My personal belief is that CCSVI and MS do indeed have a relationship, at least in some MS patients. However, I acknowledge that my opinion is based primarily on anecdotal evidence, and anecdotal evidence alone is not enough to state anything with scientific certainty. Despite the insistence of many in the CCSVI advocacy community, the link between CCSVI and MS has not yet been established with evidence that measures up to the scientific standard. On its face, the basic premise of CCSVI, that restricted blood flow through the central nervous system, caused by vascular abnormalities that are very likely congenital, slowly cause damage to the CNS over the course of decades, eventually becoming significant enough to result in a clinical diagnosis of Multiple Sclerosis, seems simple and makes perfect sense. Yet upon closer inspection, the picture is not quite so clear-cut.
There have been several very convincing studies demonstrating that venous abnormalities now known as CCSVI occur more often in MS patients, and even in patients with other neurologic diseases, than in healthy control subjects. Conversely, there have also been quite a few studies disputing this. Almost all of these studies, pro and con, have relied on noninvasive imaging techniques (Doppler ultrasound or MRV) to ascertain the presence of these abnormalities. Unfortunately, neither of these noninvasive imaging techniques has proven to be entirely accurate, though Doppler ultrasound, in the hands of a skilled and well trained technician, does appear to be the more reliable of the two techniques. Still, we have research groups reporting widely divergent findings, and some of that divergence could possibly be attributed to the relative inaccuracy of the diagnostic methods being utilized.
Complicating matters further is the fact that human venous anatomy, with a few exceptions, has been very little studied. So little, in fact, that no clear-cut definition of "normal" exists when it comes to the anatomy of the veins that drain the central nervous system. It had previously been assumed that since the veins in question had so many built-in redundancies, any blockages encountered would be easily compensated for. While the Interventional Radiologists performing the CCSVI treatment procedure are reporting that the overwhelming majority of MS patients are indeed displaying a large number of venous abnormalities, we cannot state with any certainty that a significant portion of the healthy population does not also present with such abnormalities.
What are desperately needed are trials using catheter venography to ascertain the prevalence of CNS venous abnormalities in healthy control subjects. However, there are some ethical questions involved in performing this minimally invasive procedure simply for research purposes. Although the risk is low, catheter venography, like any invasive procedure, does carry with it the potential for dangerous complications, and the prospect of exposing healthy subjects to these risks has inhibited such studies from taking place. Until it can be established beyond dispute that vascular abnormalities in the jugulars, azygos, and other veins that drain the CNS are more prevalent in MS patients than in the general population, the question of the CCSVI/MS relationship will not be put to bed.
Let's assume, though, based on the anecdotal reports, that there is a connection between CCSVI and MS. The big question then becomes whether CCSVI is the cause of the disease, or an effect of the Multiple Sclerosis disease process. Again, there is enough conflicting data to support both sides of the argument.
Those who support CCSVI as the cause of MS site several compelling reasons for their belief. One of these is that many of the abnormalities being seen in the veins of MS patients, such as anomalous membranes and fused valves, appear to be congenital in nature, that is, patients have had them since birth (click here). If these defects are congenital, and occur in greater preponderance in MS patients than the healthy population, it would seem reasonable to assume that they play a causative role in MS disease etiology. Another argument in favor of CCSVI as the cause of MS is the growing body of evidence that suggests that nervous system tissues in MS patients are damaged before the immune system comes into play (click here for one such study), findings that would seem to contradict the prevailing theory of MS, the "autoimmune theory". The autoimmune theory states that, for reasons unknown, the immune systems of MS patients go rogue and start attacking the patients' own central nervous system tissues. If some studies done within the last decade are correct, and CNS damage occurs before immune system involvement, this would apparently discredit many of the basic assumptions of the autoimmune theory, and CCSVI provides an explanation as to how this damage occurs.
While I've long held the autoimmune theory in contempt, and I'm convinced that the aberrant immune response seen in MS patients is a symptom of some larger underlying and as yet undiscovered cause, I'm not sure that cause is CCSVI. While the CCSVI hypothesis does in some ways elegantly account for some of the mysteries surrounding MS (the venocentric nature of MS lesions, the reduced volume of blood flow through MS brains, etc.), it does not account for several of the more confounding aspects of the disease. It's difficult for CCSVI to explain the geographical distribution of the MS population, which sees a far greater prevalence of MS the further away one gets from the equator (click here). Related to this geographic distribution, CCSVI also can't explain some of the migratory observations made in regard to disease prevalence (click here). When a person below the age of 15 migrates from an area of higher disease prevalence to one of lower prevalence, they take on the characteristics of their new home. When the migrant is over the age of 15, though, they retain the propensity for the disease of the area they migrated from. In other words, a person under the age of 15 migrating from Maine (high prevalence) to Florida (low prevalence) has the same low chance of getting the disease as a Florida native. However, older migrants retain the higher chance of getting the disease seen in Maine. Furthermore, children of these older migrants, born after the move south, take on the same lower chance of developing MS as children born to the native population.
Similarly, CCSVI cannot account for the existence of "MS clusters", which are small concentrations of population in which MS appears to be epidemic (click here). The most famous of these clusters is in the Faroe Islands, an island group situated between the Norwegian Sea and the North Atlantic Ocean. Prior to World War II, MS was virtually unknown among the native islanders. During World War II, the British, who have a high incidence of MS, occupied the island, and subsequent to this occupation, MS has become epidemic among the native population. Another such cluster was recently identified in a small town in Ohio, where over two dozen MS cases were discovered within a six block radius.
The geographic and migratory components of MS epidemeology, as well as the existence of MS clusters, are heavily suggestive of an environmental (infectious or toxic) element to the MS disease process, and indeed, recent studies have linked several viruses, most of them in the herpes family, to MS. Just within the last week or two, a study out of Taiwan, which looked at hundreds of thousands of subjects, found that people suffering an outbreak of shingles, a painful skin condition caused by the varicella zoster virus (which also causes chickenpox), are three times as likely to develop MS within the year as those who didn't suffer from shingles (click here). Likewise, the Epstein-Barr virus has also been cited as a possible infectious trigger of the disease, with some scientists stating that if a patient isn't infected with EBV, they won't get MS (click here).
Another potential problem with CCSVI as the cause of MS is the inflammatory patterns seen in patients afflicted with the disease. According to CCSVI theory, disrupted blood flow through the CNS creates damage and inflammation to the cells contained within, through a variety of possible mechanisms. This would lead one to expect that the longer the condition persisted, a patient's levels of inflammation would slowly increase over time, in a steady upward slope. However, in reality, RRMS patients see their greatest amount of inflammation early in the disease, during its relapsing remitting stage. Once the disease moves into the progressive stage, and RRMS turns into SPMS (normally within 10-15 years when left untreated) inflammation levels decrease dramatically. Patients with PPMS, who start out with progressive disease, very often show very little signs of CNS inflammation. As a matter of fact, this lack of inflammation, seen as enhancing lesions on MRI images, is a hallmark of progressive disease. This is why anti-inflammatory therapies such as steroids generally have little effect on patients with progressive illness.
Of course, none of this directly contradicts the idea that CCSVI may play some causative role in the disease of some MS patients, but it strongly argues against the idea that CCSVI is the primary cause of the disease.
Some compelling evidence that CCSVI may be an effect of MS has been presented by several researchers, most notably Dr. Robert Zivadinov and the researchers at the Buffalo Neuroimaging Analysis Center. Although Dr. Zivadinov's findings have been savaged by some of the most fervent "CCSVI as cause" proponents, the totality of the research done under his direction does point to the possibility that at least some of the venous abnormalities now called CCSVI are a result of the MS disease process. Although Dr. Zivadinov's opinions only recently made headlines (click here), he in fact implied them in research presented in October, 2010 at the annual ECTRIMS (European Committee on Treatment and Research in Multiple Sclerosis) conference. One paper presented at that time demonstrated that the severity of CCSVI increases with the severity of Multiple Sclerosis symptoms experienced by patients, and with a more advanced disease course (click here). These findings were backed up by papers presented by researchers from Beirut (click here) and Italy (click here). Another study presented by Dr. Zivadinov found that subjects who presented with CCSVI had significantly more lesions and brain atrophy as measured by MRI than those MS patients without vascular abnormalities (click here). Yet another investigation presented by Dr. Zivadinov looked at the correlation between a gene implicated with MS, and CCSVI, and found that the data supported an association between MS disease progression and CCSVI separate from the suspect gene. The implications of these findings are that CCSVI could be a risk factor in developing the disease, or a result of the progression of MS (click here).
Additionally, it would seem to me that the high rate of restenosis in patients who have undergone CCSVI treatment venoplasty could also hint that CCSVI is more an effect rather than the cause of MS. Despite the wide range of treatment methodologies being employed, patients are still experiencing a re-narrowing of their previously unblocked veins far too frequently. This has been seen even in patients who have had stents placed in their veins, only to see their veins stenosing in areas not stented. If CCSVI were an effect of the MS disease process, one would expect to see repeated restenosis of the veins as that disease process continued to impact a patient's vasculature.
So then, what conclusion can be drawn? Is CCSVI the cause of MS, an effect of the disease, or does it have no relation to Multiple Sclerosis at all? My honest belief is that the answer could be all three, depending on the individual patient.
Multiple Sclerosis is a remarkably heterogeneous disease, meaning that it impacts different patients in vastly different ways. Across the wide spectrum of MS patients, the primary symptom of the disease may be fatigue, cognitive dysfunction, muscle weakness, spasticity, eye trouble, nerve pain, or any combination thereof. Some patients can have the disease for decades and show very little physical disability, while others find themselves in a wheelchair (or worse) in less than 10 years (sometimes much less). Some patients have a great many lesions and very little disability, others have few lesions but devastating disability. Confounding the issue even more, MS comes in several different flavors, from Relapsing Remitting to Primary Progressive, and evidence suggests that the disease process at work in progressive disease may be quite different than that underlying Relapsing Remitting MS.
Given such a wide array of disease presentations, and thus the likelihood that a variety of mechanisms may be at play, it could very well turn out that CCSVI plays no role at all in the disease of some patients, a more causative role in the disease of others, and could be an effect of MS in yet another patient population. Very likely the line between cause and effect may be quite blurred, with CCSVI playing an exacerbating role in a disease that almost certainly has, in addition to a vascular component, very strong genetic and infectious components as well. The mix may be dramatically different from patient to patient, and indeed, CCSVI may be THE major factor in the disease of some patients, but play absolutely no role in the disease of others.
This may be reflected in the breakdown of outcomes reported by some of the Interventional Radiologists doing the CCSVI treatment procedure. The most widely quoted is Dr. Gary Siskin, of Albany New York, whose group has done over 700 procedures. Dr. Siskin has found that one third of his patients experience dramatic improvements, another one third experience mild improvements, and a final one third experience no improvement whatsoever. Further complicating this equation is the definition of just what constitutes a dramatic improvement. For somebody who's most disabling symptom is fatigue, a lifting of that fatigue would undoubtedly be called dramatic. For somebody more disabled, like I am, a lifting of fatigue, while certainly welcome, would hardly be defined as a dramatic improvement.
As I stated earlier, clear as mud…
Once again you have given us a superlative evaluation of the science and psychology of this topic. Thanks.ReplyDelete
Peace Be With You blog
great reading as always. The Faroe Islands, however, are not in the South Pacific but in the North Atlantic (between Scotland, Denmark and Iceland).
Once again a fascinating read. The shingles connection is particularly intriguing to me as I too had the malady back in my twenties. This is something that I will certainly keep an eye on. MS is indeed a complicated disease! Thanks for the info.
Anonymous-thanks for the geography lesson, the change has been duly noted…ReplyDelete
Your thinking, organization and timely delivery is delivered good on your website. Good to have people like you on it since modern medacine made a mess of this and you can trace an inteligent history back to Mary Shelly and further to antiquity. The discourse has changed but the song remains the Same. Nice JobDelete
CCSVI is a confusing issue.
You have a way of correlating the data which allows me to understand it a bit better.
I know two people that have undergone the procedure, one has experienced great improvement, the other zilch.
The herpes, EBV connection is interesting, I have had both mono and shingles.
Thanks for the info.
I had the "gold standard" for testing--a venogram that showed 50% blockage of the azygos and 90% of both jugulars. A venoplasty was done and I can now walk without a mobility aid for the first time in over 17 years! I am very pleased to be "walking proof" that blood flow from the brain is important--even if you have been diagnosed with MS.ReplyDelete
Burnaby, BC, Canada
You are quite right in your descriptions, but from a person with MS it is irrelevant (in my opinion) whether it is "the chicken or the egg". What seems undisputed is the fact that a majority (over 50%) of all MS`rs have veins stenosed or something obstructs the blood flow. By rectifying this through a small and easy procedure a lot of the people get rid of many, many symptoms. In my opinion it is unethical to refuse patients, their family and loved-ones a possibility for a better life and future. Not to mention the cost of drugs not taken... As far as I know patients with stroke get their veins fixed. Are we with MS less "worth" or do doctors have "a ownership" to CCSVI just because they gave us the "MS tag"? Until Intervention Radiologists gets a clear "ownership" on CCSVI the other so called experts (neurologists) will try to drag this out, miss-judge and take a negative approach to this. I hope I never have to see another neurologist again.ReplyDelete
Really interesting and balanced - thanks!ReplyDelete
The very first article on CCSVI that is clear on what is going on in the research field; very well written and easy to grasp. Like yourself I have MS and am blogging (only started though :D).ReplyDelete
Keep up the good work and the positive vibes, you've got a brand new fan here! :)
Once again you have used your time so generously in breaking this all down for newbies and "know it all" folks alike.
I, for one, have always believed that "MS" is a landfill diagnosis that lumps us all together. I think that it is just a matter of time, perhaps a LONG time, before someone figures out that we have different diseases with different etiologies and best-practice treatments.
Thanks for taking so much time to explain, AND link to supporting evidence, your well thought out analysis.
You are a gift to us all!
As always Marc, great blog. They may never figure out this one I'm afraid. We need to advocate for ourselves and do what we think is best. You have given us the information to ignite the desire to know more.ReplyDelete
My daily poem linked to this fabulous post.ReplyDelete
Nicole, I agree. I have long thought the diagnosis process for MS was logically weak. A diagnosis saying "it's not A and it's not B therefore it must be C" leaves a lot of unknowns. With different presentations and progressions, I always thought it odd to assume everything currently thought of as MS belongs under the same umbrella.ReplyDelete
Great blog article Marc and a great example of why you are so deserving of the "Top Health Blogger" award!ReplyDelete
All I know is that I had the procedure done and it has dramatically changed my life. I am cane, pain, fatigue and cog~fog free [I think LOL].ReplyDelete
I will leave the scientific proof to those of a higher intelligence.... I will just go with what works for me.
As to what causes what, why, when and how....all I care is who it works for and the answer to that is me and maybe you.
Marc, as always a fine piece of writing.
I'm still curious about the role of physical activity in CCSVI and MS. Obviously (and from my own experience) the more active the disease process, the less likely you are to be physically active. Does this lead to the blocked vein thing? Is part of the reason for recovery the increased activity of the patient?ReplyDelete
My other questions surround the newly discovered changes in the grey matter of the brain and whether they are more important than first thought. Are those changes explained by blocked veins?
And finally, if there is increased pressure in the veins, why don't I have rosacea, or ruptured capillaries in my face? Still find that confusing...
Very interesting post, especially the shingles part... I never actually had it, but I felt some of its symptoms (skin sensitivity and warmth running through half of my body, though no pain). 4 months later I had my first major relapse, which led to my diagnosis.ReplyDelete
As always, amazingly written, love your blog! greetings from Argentina
Well I for one agree and feel that 'CCSVI' is not 'the' cause - I believe it's an effect of a different problem that's affecting the veins. But no, not the root so to try and fix it will only be a temporary patch. Albeit a welcome one for some and a disastrous one for others.
I have always said from day one when getting the usual pooh-poohing from a neuro' and he asked, "well what do you think it is causing this (MS and CFS) then?"
I said, "For a start, I don't have either because they mean nothing. You don't know what either are, why they vary so much or what causes them, they're just a label for a huge variety of symptoms. But if you genuinely want to know (he didn't) I 100% believe my problems stem from low lying viruses tests can't spot that have control of my immune and nervous system and a big problem with my circulation possibly caused by them."
That was 11 years ago when I was 20, and I still believe the same thing.
Thanks for a great summary,
'Interrupted' from TIMS
Thanks for the great summary.ReplyDelete
Although ultimately we will want to determine the causal link (if any) between MS and CCSVI, I still find it amazing that there is reluctance to pursue the Liberation treatment in many places - including here in Canada.
You mention that Dr. Siskin has done over 700 procedures, surely enough to provide statistical significance, and I have seen similar or better results from clinics in eastern Europe.
If a treatment was found that provided "dramatic improvements" for one third of patients in any other disease, and incidentally is inexpensive and has been shown to have low risk, would the medical establishment not be racing to provide it to patients? What is it about MS that leads otherwise objective physicians and scientists to call the treatment snake oil?
I sure don't know, but I hope they get over it soon.
John Robert said, "What is it about MS that leads otherwise objective physicians and scientists to call the treatment snake oil?"ReplyDelete
Gosh, I hope it's not the ghastly amounts of money everyone is making on our condition. Take a pill, take a shot, get infused, and remember to do this over and over and over again... And if you don't?? Hmmmm...you might get worse. Boo!
John Roberts asked, "What is it about MS that leads otherwise objective physicians and scientists to call the treatment snake oil?"ReplyDelete
Prescribe a shot. Prescribe an infusion. Prescribe a pill for walking. Prescribe a pill to stop peeing. Prescribe physical therapy. Prescribe occupational therapy. How about an AFO, then a walker, then a scooter, then a chair?? Did I mention lifts? ramps? Hand control for cars? Adaptive vehicles?
If they find a cure, a LOT of folks will be kicked off the MS gravy train.
Consider our disease a public service or our way to help the economy thrive.
Thanks so much for your, as always, excellent summary and analysis of such a large and difficult subject. I'm put off by the rhetoric of so many CCSVI advocates, but I know I can always trust you for a fair and balanced discussion supported by facts.ReplyDelete
Thanks for the very kind comments, everybody. I'm glad that so many find this blog to be of help.ReplyDelete
Dabble-just wanted to answer your questions as best I can. It appears that many of the venous abnormalities being found are congenital, so I don't think a lack of mobility we create the problem, but it certainly might exacerbate it. Changes to gray matter can be explained by blocked veins, in that those blockages slow down the flow of blood through the brain and spinal cord, and over the course of decades this can lead to cell death and tissue atrophy, which is indeed what is seen in multiple sclerosis. As far as your not having rosacea, the veins in question drain the central nervous system, and are a different system than the vascular system that services the skin on your face.
HI you might want to look at this link, if you haven't alreday. http://www.medpagetoday.com/clinical-context/MultipleSclerosis/31868Delete
Hi MArc - thanks for your comments. I have not seen many studies that support the congenital blocked veins leading to MS hypothesis. Yes, there are some young folks with "blocked veins" but the anatomy of a vein is such it is difficult to prove blockage (as they open when needed) and the other issues is that no one has yet proven these alterations in anatomy are pathological. There is also a lack of proof that there is a lack of blood access to the brain as this would result in greater pathology than what we see - think of the results of a heart attack or angina, for example. I just haven't seen such studies - if you have I'd love to see them.ReplyDelete
Regarding the venous drainage thing, we are talking of jugular vein drainage which drains a great deal of the head, not just the central nervous system. Check out the anatomy. If you are going to argue that I don't have rosacea because of collateral drainage, what's to say the same drainage isn't available for the brain? In fact, it IS available, and for those who have blockages. it usually pitches in quite well.
The problem is that the very techniques that we use to assess the blockage are techniques that can cause it to "appear".
I don't mean to sound cranky - yes, I do wish this all was true and we could all believe in a magic cure, but it isn't helpful to use incorrect anatomy and sloppy studies to create false hopes. I am so sad for those who have had the "treatment" and not benefitted and then lost their life savings enroute.
Incidentally, I'm just as skeptical of drug studies - and I'm not talking out of my hat as neither are you - my background is as a nurse and epidemiologist (I study patterns of health and disease) and am a studies skeptic since I know how results can and are tweaked - god help me I've done so myself.
Dabble-just to be clear, while I am a "believer" in CCSVI, I'm certainly a skeptical believer. Many of the venous abnormalities being described by the interventional radiologists doing the procedure would appear to be congenital in nature. The physicians are seeing lots of fused or improperly formed valve leaflets, and/or anomalous membranes, weblike structures, and septums in the effected veins. It would seem that abnormalities such as these would be congenital. Of course, there are also many instances of simple venous stenosis, which of course could fall within "normal" parameters, or be a result of the MS disease process. I was surprised to learn that the CNS venous system had been so little studied that no real definition of normal exists. This is, of course, quite a problem…ReplyDelete
Thanks for correcting my assumption about the internal jugulars, I was under the impression that the blood flow through the facial areas was handled by the external jugulars. Upon doing some research, it appears to be a shared responsibility.
The CCSVI hypothesis postulates that slowed perfusion through the brain, over the course of decades, is responsible for the damage that eventually reaches a clinical level and is called MS. Therefore, one wouldn't expect to see dramatic pathology if the hypothesis were correct, as the disruption in blood flow would be rather subtle. Brain atrophy and reduced blood flow through the CNS are established hallmarks of MS. The standard view is that, because the MS brain undergoes atrophy, less blood is needed, resulting in the observed reduced blood flow. CCSVI advocates claim that this process is actually reversed, and reduced blood flow leads to brain atrophy.
At this point, only time will tell just how valid the CCSVI hypothesis turns out to be. A recent review of the available published research, in addition to some preliminary data from the MS society sponsored trials, has led the Canadian government to move ahead with CCSVI treatment trials, as the findings indicate a correlation between CCSVI and MS. They will be very interesting to find out just what these MS society studies are finding.
There are currently studies to support both sides of the argument, and you're absolutely correct in stating that the noninvasive methods used to detect venous anomalies by many of the studies are far from foolproof. I share your skepticism of medical studies in general, as I too have first-hand knowledge of how easily data can be tweaked. I worked for a time in market and political research, conducting polls often used by the major news operations. Changing a word or two in how a question is asked can easily skew the results one way or the other, and most of the data involved in MS studies is obtuse enough to be interpreted in any number of ways (and is usually interpreted in a manner that is beneficial to the sponsor of the study)…
On final followup -ReplyDelete
The Canadian government is funding trials of the treatment not because of any additional proof but rather because of political pressure. Several of the provinces have already bowed to the pressure and are saying they are funding trials - but they are having a dickens of a time creating a study protocol that will be valid. Saskatchewan, for example, has been looking at a framework for the past 6 months and have not been able to identify one. I live up here and I'll tell you it is a battle for resources, so before we dedicate $$ to anything, it has to be proven.
I think the best idea for now (though not providing proof) would be to create a registry of people with MS, identify an actual test for things such as strength and etc that are now being verbally reported (these tests do exist - say the sit to walk test, but they don't seem to be common in the MS clinic assessments for some reason.) and start actually evaluating outcomes.
It IS astonishing no one has looked at veins much before, isn't it? My ex grandfather in law was an anatomy professor and even his text (Last) is sketchy on things. I suspect it's because they are very hard to evaluate in cadavers as they deflate and are thin walled.
Marc, thanks so much for a clearly defined exposition on the state of the CCSVI field. It's very useful to have you synthesize all of the studies for us.ReplyDelete
I'm still uncertain about what this means given my own experience. I underwent an MRV at Stanford and was told I had 90% blockage in both upper jugulars. I saw it myself on the scans, including a very large collateral vein system! Several months later I had two IR doctors in my home state look at the scans and they saw it too. One of them performed a venography with the intention of using balloon angioplasty to open up the blockages. Except when the Doctor got in there with the catheter and released the dye the blockages appeared to be gone. What does this mean? The doctors had no answer. Since my MS is mild and in remission with drugs I can tolerate I sit back and wait for more information as I am lucky to have time on my side. Some day I will go back and have another doctor look again. Maybe they will no more then.