Finally! Canadian Government Decides to Fund CCSVI Treatment Trials…

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In a surprise move, the Canadian federal government has reversed its previous decision, and decided to fund CCSVI treatment trials on MS patients (click here). Just last year, government officials decided against funding such trials, citing a lack of evidence that a clear link existed between CCSVI and MS. Now, a working group of scientific advisors, after reviewing already published research in addition to the preliminary data from the seven ongoing studies funded by the MS societies of Canada and the USA, has concluded that there is enough evidence of a relationship between the vascular abnormalities collectively known as CCSVI and Multiple Sclerosis to warrant federally funded treatment trials (click here).

This is extremely welcome news to MS patients worldwide. Although treatment trials won't answer many of the scientific and medical questions surrounding the CCSVI hypothesis, such trials will determine whether catheter venoplasty, when used to open blocked veins and improve impeded bloodflow through the central nervous system of MS patients, results in an improvement of symptoms and/or a slowed progression of the disease. While academic questions such as cause and effect ultimately must and will be answered, the most pressing issue for MS patients themselves is whether or not getting treatment for CCSVI will improve their symptoms and lessen the long-term impact their potentially crippling disease.

What's of primary importance now that a mandate has been given to commence treatment trials is the design of those trials and exactly which treatment protocols will be used on the patients enrolled in them. Over the last 18 months we've learned that treating CCSVI is far less simple than was originally thought, and the physicians most experienced in the treatment of CCSVI are in unanimous agreement that the learning curve involved with perfecting the technique is steep, and the methodologies used are still a work in progress. The fact is that many of the treating physicians use quite disparate treatment protocols, and there is no clear consensus on best practices and a standardization of treatment methodology.

As CCSVI treatment has thus far been unavailable in Canada, there is an absence of Canadian physicians experienced in the treatment procedure. I trust that the scientists involved in the Canadian trials are fully aware of such issues, and that the physicians who will be performing the treatment procedures will undergo training at the hands of the experienced physicians outside of Canada who have been blazing the trail in performing what is still an experimental procedure. It's vital that these trial procedures be done using the latest and most effective techniques, as sub-optimal procedures will lead to sub-optimal results, which would be disastrous for the advancement of the science, and could easily lead to false conclusions about the effectiveness of treatment.

I would expect that the Canadian trials will not only demonstrate whether CCSVI treatment is effective, but, if it is, which symptoms are most impacted by improving venous blood flow, and which patient populations stand to most benefit from CCSVI treatment. MS is an extremely heterogeneous disease, with no two patients experiencing the malady quite the same way. A recent study (click here) by a CCSVI treatment practice in Poland found that patients most likely to benefit from CCSVI treatment are younger females (under the age of 30) with Relapsing Remitting Multiple Sclerosis, who have had the disease for relatively short amount of time and have not yet experienced severe mobility issues. Keeping in mind that the study was based on a relatively small sample size (47 patients), and the long-term effects of successful CCSVI treatment are still unknown, such data does make some sense in the context of what is known about MS pathophysiology, especially once the disease moves from its relapsing remitting form into its progressive stages.

Recent evidence has provided tantalizing clues that suggest that the progressive stages of the disease may be driven by an abnormal immune response contained entirely within the central nervous system, in a sense approximating a rogue immune system that operates separate and apart from the systemic immune system at work in the rest of the body (I'll blog about this in the near future). The implications of these findings, if correct, are profound, and would suggest that once the disease enters its progressive stages, treatments that are effective in RRMS, even CCSVI, may be rendered useless, as they do nothing to address an aberrant immune response that is contained entirely behind the blood brain barrier, operating independently and completely unto itself.

Be that as it may, the MS community on the whole should loudly applaud the Canadian government for taking the bold if belated step of federally funding vitally important CCSVI treatment trials. At the very least, such trials will pry scientific attention away from its current togmatic insistence that MS is strictly an autoimmune disease confined only to the central nervous system, and see it as a systemic problem with physical implications reaching beyond the brain and spinal cord. For far too long the autoimmune model of the disease has ruled the day, generating billions of dollars of profit as it turned the treatment of Multiple Sclerosis a hugely lucrative business, while at the same time generating tangible but limited benefits to patients suffering from the disease. Let these Canadian trials be a huge step towards a new understanding of the MS, one that will lead to its final eradication and an end to the suffering of millions of patients worldwide.

CCSVI and MS: Cause, Effect, or Neither?

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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…

Related articles

• The Rorschach test of CCSVI research (macleans.ca)
• Higher CCSVI rates with MS, but findings still unclear (ctv.ca)

CCSVI As Punk Rock

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I Want To Be Anarchy.

This was the battle cry of a generation of young rock ‘n rollers, who, in the late 1970s, donned black leather jackets, cut their hair short and spiky, picked up instruments they barely knew how to play, and declared war on a bloated music industry establishment. Sick of having music shoved down their throats by corporations that had become self-reverential and complacent, they decided to take matters into their own hands, and by doing so changed the course of rock 'n roll history.

After the incredibly vibrant and creative 1960s, which saw rock 'n roll evolve from a teenybopper fad into a multifaceted and sometimes profound art form, by the mid-1970s music seemed to be suffering from a particularly brutal hangover. Dominated by bands that had become behemoths, and musicians who had come to view themselves as royalty, rock 'n roll had changed from the soul of a youthful revolution to the sound of cash registers opening and closing. Sure, there were exceptions, but they were few and far between, followed by pockets of ardent fans but stuck in relative obscurity. Record companies barely supported the likes of David Bowie, Iggy Pop, The New York Dolls, and T Rex, preferring instead to throw their money and marketing might behind safer, less challenging acts, but in doing so stripped the passion out of an art form that had been born of it.

The Multiple Sclerosis establishment found itself in a vaguely similar position in 2010. Prior to the late 1980s, decade after decade of investigation had been spent making absolutely no headway against the disease, despite the best efforts of researchers. These were the dark ages, a gloomy time for patients diagnosed with MS, during which the disease was considered a "diagnose and adios" malady. There was precious little doctors could do for their desperate patients except wish them well. Researchers primarily concentrated on looking for an infectious cause to the disease, with a few suggesting that the vascular system may somehow be implicated. Despite the occasional report of a breakthrough, none ever panned out, and patients and their doctors were left with little option other than to simply watch the disease take its insidious toll.

In the 1980s, things changed. The theory of autoimmunity, which posited that for reasons unknown a patient's own immune system goes on a cannibalistic attack, destroying a body's own central nervous system tissues and resulting in the telltale signs of MS, took hold and started to grow roots. By the late 80s a substance known as beta interferon, thought to somehow modulate aberrant immune systems, was in full clinical trials on MS patients. These trials proved successful, even if only moderately so. A statistically significant percentage of patients with relapsing remitting disease were shown to suffer less relapses while on beta interferon drugs, and their MRIs displayed fewer areas of disease activity. It was hoped that this would translate into the delay or even cessation of disability progression, but at the very least these new drugs did increase the quality of life for some of the patients taking them, and physicians finally had a weapon in the fight against the disease.

As the autoimmune theory became more entrenched, MS research started focusing almost exclusively on finding better and more powerful methods of suppressing the human immune system. This led to the creation of new classes of drugs which suppress various parts of the very intricate and not fully understood immune system, substances which show more efficacy than the interferons in treating the symptoms of MS, but also carry with them the specter of serious and sometimes deadly side effects. While these drugs, too, have had a profound effect on the quality of life of some of the MS patients taking them, none address the still unknown root cause, or causes, of the disease. Problematically (for patients hoping for a cure, at least), MS drugs have become financial blockbusters, transforming multiple sclerosis into an $8 billion a year industry, a financial windfall which has further focused the attention of researchers on tinkering with the immune system rather than finding out just what causes it to suddenly turn upon the body’s own cells.

Back in the late 70s, restless kids fed up with the pablum being pumped out by the music industry (appropriately dubbed "corporate rock") started to create their own music. Though their output may have been technically less than masterful, the raw passion, emotion, and soul poured out by bands such as The Sex Pistols, The Clash, and The Ramones more than made up for their musical deficiencies. Combined with sarcasm, swagger, and a loud disdain for the mainstream (one of the seminal albums of the time, by The Dead Boys, was appropriately entitled "Young, Loud, and Snotty"), the brashness of these young punks was startling, and set the mainstream back on its heels.

Their popularity primarily still confined to the musical underground, the antics, in-your-face behavior, and outrageous attire of the early punks soon grabbed the attention of the media, who at first treated them with derision, as did the corporate giants the punks were attacking. Initially shrugged off as troublesome outcasts, many pundits predicted their quick demise. Instead, punk thrived and only gained in popularity, spawning a vibrant counterculture whose ethos spread from music into the visual and cinematic arts. Due to the popularity of a new communications entity, MTV, punk music and fashion spread quickly from the cities to the suburbs, and soon the major labels were scrambling to sign and market their own punk bands, now labeled under the more palatable moniker of "New Wave".

Late in the first decade of the 21st century, the Multiple Sclerosis establishment likewise found itself confronted with a radical new idea, called CCSVI. This hypothesis, first put forth by the Italian vascular surgeon Dr. Paolo Zamboni, states that blockages in the veins that drain the central nervous system either cause or contribute to the neurodegenerative disease we know as multiple sclerosis. Furthermore, Dr. Zamboni's initial trials showed that opening these blockages, using a relatively simple and minimally invasive procedure, seemed to dramatically relieve the symptoms of MS, suggesting an entire new avenue of investigation into the disease. At first, Dr. Zamboni's findings got very little attention, outside of a small group of patients keenly debating the relative merits and demerits of the idea on a small Internet MS forum. Soon enough, though, the Canadian media picked up on the story, and all hell broke loose.

Rather than approach the idea with open-minded scientific curiosity, the MS establishment initially tried to dismiss the idea of CCSVI as absurd, some going so far as to label it a "hoax". MS patients reacted with indignant fury, the pent-up frustrations of years of being treated with hyper expensive and nominally effective treatments that do nothing to address the essence of what's making them sick exploding like Krakatoa, creating a medical tsunami the likes of which had never before been seen. Carried along by new social networking tools such as Internet patient forums, blogs, and Facebook, the MS establishment could do nothing to harness the growing CCSVI movement, a patient driven initiative that forced the issue as patients took matters into their own hands and began traveling abroad in pursuit of CCSVI treatment. In the United States, Interventional Radiologists, the doctors who specialize in the catheter procedures used to treat CCSVI, soon started taking notice, treating MS patients for the blockages that were indeed been found in their veins. Though far from universally successful, anecdotal evidence does seem to indicate that treating CCSVI does, at the very least, relieve some of the symptoms experienced by some MS patients.

As the 1980s evolved, punk evolved with it. While mainstream rock acts still commanded a lion's share of attention, new bands, deeply influenced by the original punk rockers, burst onto the scene, and gained in popularity. Slowly, what once seemed cacophonous, outrageous, and even obscene began to be absorbed into the mainstream, and the lines that separated rock 'n roll genres began to blur. Though the revolutionary vitality felt by those in the center of the storm in the late 70s and early 80s was largely gone, and punk rock's fangs had been filed down, by 1993 punk reigned supreme as it flooded the airwaves and music stores under the new banner of "Grunge", a development that the leather jacketed, safety pinned, and spiky haired kids 15 years before could never have even imagined. These days, the children of the original punks listen to modern music that would not exist if it weren't for long gone bands that they've barely heard of, largely unaware of the history behind the music.

The future of CCSVI is likewise beyond prediction. There is much still to be learned, both about the condition itself, and how best to treat it. The significance of CCSVI in the big picture of MS still needs to be determined. Despite the hopes of the most fervent CCSVI supporters that it will prove to be THE cause of MS, and the doubts of the naysayers who claim it has no significance at all, the truth will likely fall somewhere in between, and could very well vary from patient to patient. For some, CCSVI may play a dominant role in their disease, for others it may play no part at all. Current treatment protocols need to be standardized and perfected, as we currently see too many problems with restenosis, clotting, and the occlusion of treated veins, but eventually these issues too will be worked out.

Perhaps what's most important, though, is the tremendous upsurge in patient self-advocacy, education, and empowerment that has been the product of the intensity of the CCSVI debate, which has quite possibly changed forever the dynamic of the patient-doctor relationship. No longer will we as patients be dictated to, but partnered with. Knowledge that was once the province of an anointed few is now open to the masses, a development with repercussions that may take many years to resolve. New generations of doctors will undoubtedly be more open to this changing dynamic than the old guard, but Pandora's box has been opened, and for a while, it seems that anarchy will have its day. Punk rock and CCSVI, Viva La Revolucion!

Related articles

• The Rorschach test of CCSVI research (macleans.ca)

Bits and Pieces: Back, Once Again

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Here's yet another edition of Bits and Pieces, in which I assemble various MS related (and sometimes non-MS related) materials for your reading and/or viewing pleasure. These are all items which have piqued my interest for one reason or another, which I feel the compulsive need to share with my loyal (or even disloyal) readers. I hope these items pique your interest also, as having one's interests piqued can really be the peak of one's day.

I use voice recognition software to "write" these posts, so in actuality I speak to them, and for some reason I'm experiencing much merriment when speaking the word "piqued", in addition to the fact that I think it's pretty neat that the software is differentiating between piqued and peaked and peeked. Okay, so I had to help it out that with that last bit, but it's entertaining me nonetheless…

Anyway, let's get on with it. Here's a peek at what has piqued my interest over the last couple of weeks. To the right is a picture of a pique peek peak.

• CCSVI stuff: the International Society of Neurovascular Disease convened a meeting of some of the foremost CCSVI experts on March 14-15, in Bologna, Italy. Much important data was presented, including studies on the epidemiology of CCSVI and MS, the role of oxygenation and tissue drainage, the role of iron, advanced diagnostic imaging, the treatment of CCSVI, and development of animal models of CCSVI. Dr. Paolo Zamboni, who first put forth the CCSVI hypothesis, demonstrated new technology designed to improve the ease and accuracy of diagnosing CCSVI, in the form of a collar that can be placed on a patient's neck, which measures the difference in the volume of blood going through the jugular veins when measuring patients in an upright and then supine position. (Click here) for a summary of the conference findings, which will open up as a Word document. In my version of Word, the document opens up in a multipage format that makes it difficult to read. If you experience the same problem, simply go to the "view" menu and choose the "one page" option.

  From March 26-31, the Society of Interventional Radiology (SIR) will hold their annual meeting in Chicago, at which CCSVI will be a major topic of discussion. On the evening of Tuesday, March 29, the CCSVI Alliance will be holding a Doctor's Roundtable Discussion on CCSVI and MS, which will be open to the public. The panel includes a long list of some of the most notable names in CCSVI research and treatment, and the discussion, which will include questions from the audience, should be absolutely fascinating. Anyone in the Chicago area with an interest in CCSVI should make every effort to attend. (Click here) to register for this free event.

• Researchers at Purdue University have discovered that the decades-old hypertension drug Hydralazine may delay the onset and reduce the severity of MS symptoms (click here). The scientists theorize that the drug works by blocking the action of a toxic compound called acrolein, which is found in automobile exhaust and cigarette smoke. Coincidentally (?), a few years ago the anti-hypertension (high blood pressure) drug Lisinopril also showed promise in the fight against MS (click here). Might the action of these two drugs, both of which regulate blood pressure, play into the CCSVI hypothesis? Common sense would seem to indicate so, but common sense would also lead you to believe that both of these drugs, having long ago been proven safe, would at this very moment be undergoing exhaustive testing to ascertain just how effective they could be in treating the scourge of Multiple Sclerosis.

  Unfortunately, both drugs are so old that they are off patent, meaning that they are very cheap and available as generics. Thus, pharmaceutical companies can't make gazillions of dollars marketing them to MS patients. Since most of the medical research in this country is funded by Big Pharma, which only throws money at research that has the potential of turning a huge profit, these drugs have a snowball's chance in hell of being given more than a cursory glance as possible MS treatments. In regards to studies into Lisinopril, the lead researcher, Dr. Steinman, had this to say:

  "Who's going to pay for it?" he asked. A standard proof-of-concept study with about 200 patients would cost in the vicinity of $20 million. ACE inhibitors are as inexpensive as any prescription drug at this time, so pharmaceutical companies won't see any profits from financing a study, he said.

  The line to the vomitorium starts behind me.

• On a much happier note, many people don't realize it, but service dogs aren't only for the blind. These amazing pooches can be of considerable benefit to disabled MSers, as they can be trained to do a variety of tasks, including retrieving dropped items, turning on lights, pulling wheelchairs, preventing falls, and helping to combat depression. All that, and as part of the package you get a fuzzy best friend for life who will love you unconditionally. For more information, (click here).
• A new online magazine, Atrium (click here), is dedicated to helping shift the thinking of a new generation of doctors and healthcare practitioners in this emerging age of widespread access to information and Internet social networking. These two factors are changing the patient-doctor dynamic, which in turn should change the way that medicine is practiced. Started by two extremely motivated Yale medical students, Atrium features articles, insights, and opinions on a wide variety of subjects, including not only medicine but also art, music, and philosophy. The editors have decided to include some Wheelchair Kamikaze essays in the mix, and I'm honored to have been chosen to represent a patient's point of view. I'd urge everyone to check out this new online resource, skipping over my essays to read the wealth of other fascinating material Atrium has to offer.

• Readers of Wheelchair Kamikaze know of my fondness for photography, and I recently came across the story of Flo Fox, a photographer who was born partially blind and later developed Multiple Sclerosis, which robbed yet more of her vision as well as her mobility. In the 1970s, Flo Fox was a personality in the edgy downtown New York art scene, and had gallery and museum shows around the world. She rubbed elbows with Andy Warhol, appeared on late night talk shows, and was even featured on "Live, with Regis and Kathy Lee".

  By pure happenstance, Flo Fox appeared in a 2010 documentary about Joan Rivers, when Ms. Rivers delivered food to Fox's apartment while doing volunteer work for the group God's Love We Deliver. Now in her 60s, Fox lives in housing for the blind, but maintains her moxie and mischievous spirit. Looks like I'm only following in her wheel tracks, as it seems like Flo Fox was the original Wheelchair Kamikaze. (Click here and here) for more on the Flo Fox story, and feast your eyes on the videos below, one of which is a montage of her photos of 1970s New York City set to some very cool music, and the other a clip of her appearance with Regis and Kathy Lee, circa 1983.

Link to Blogtalk Radio Show on CCSVI

This past Monday night, I appeared on the Blogtalk Radio Internet program "CCSVI-Been There, Done That". The show featured a range of guests relating their different experiences with the CCSVI treatment procedure. The patients profiled represent a cross-section of the possible outcomes of CCSVI venoplasty, including some who saw tremendous benefit from the procedure, some who saw benefit but then restenosed, and others who saw no benefit at all. It avoids the controversy surrounding the CCSVI hypothesis itself, and puts a very human face on MS and the promise of CCSVI.

Hosted by the gracious and ever genial Amy Gurowitz, the program provides valuable patient perspectives from some who have undergone the CCSVI treatment procedure. I might be a little bit biased, as I was one of the guests, but I honestly think the program is an important listen for anyone considering CCSVI treatment. Please click the play arrow on the handy dandy interface below to listen to the show…

Edited to add: I've been getting word that some people are having trouble with the Blogtalk Radio interface, above. It works fine on my browser, but sometimes these things can be finicky. Be advised that the first minute and thirty seconds or so of the program are a commercial and then some introductory music. To play the program, you have to click on the white arrow symbol on the left side of the interface.

If the interface continues to malfunction, you can access the program directly from the Blogtalk Radio website (click here). Once on the website, scroll down until you get to the "CCSVI-Been There, Done That" section, at the bottom of which you'll find clickable buttons to play the program, along with some other options.

Sorry for the inconvenience, hopefully everyone who wants to listen to the program will be able to by either using the above gizmo, or going directly to the Blogtalk Radio website. Thanks.

CCSVI: Trying to Take the "Hyper" out of “Hyperbole"

Image by soukup via Flickr

Over the last several months, many of the Internet MS forums, chat rooms, and social networking sites have become places of sometimes heated conflict, in large part due to the extremes of emotion brought about by the topic of CCSVI. In general, open debate is a good thing, as it allows for the formation and refining of informed opinion, but in some cases, on both sides of the argument, I've seen statements presented as fact which simply aren't so, and an escalation of rhetoric that rather than adding clarity to the issue begins to obscure it.

Given the potentially dreadful outcomes of Multiple Sclerosis, and the raw emotion that such prospects engender in those that suffer from the disease, it's not surprising that disagreements can often become heated. As regular readers of this blog know, I believe there is much merit to the CCSVI hypothesis, but I'm also cognizant of the fact that the theory is likely not THE one and only answer for the majority of MS patients. For a select few it may be, but for most it is likely a piece of a very complex puzzle; just how large a piece has yet to be determined. Here then, are some of the more commonly seen hyperbolic statements made about the CCSVI and its ancillary topics, and an attempt at taking a reasoned approach to them.

"CCSVI cures MS/CCSVI is a hoax" - these are two sides of the same coin, the utopian/dystopian opinions on the subject. Let's take a look at the negative statement first, as it borders on the truly ludicrous.

When the CCSVI hypothesis first surfaced in the mainstream MS community, roughly 18 months ago, several prominent neurologists and representatives of the MS societies went on record stating that the theory had no validity whatsoever, and that patients were foolish to be wasting their time, emotion, and money pursuing the issue. These statements were made, I suppose, based on an instinctive defense of territory, and a very rigid adherence to traditional MS dogma which states that MS is an autoimmune disease confined to central nervous system, caused by an immune system that, for reasons unknown, has taken to attacking a patient's own cells. Unfortunately, this autoimmune model of the disease, which has held sway for over two decades, has done little to advance the cause of curing MS. It has, though, led to the production of a family of high-priced drugs that modulate or suppress the immune system which do increase the quality of life for a percentage of the patients taking them, but do absolutely nothing by way of offering a cure.

One would think that MS neurologists, as scientists devoted to unraveling one of the most cryptic of medical puzzles, would have their interests piqued by such an outside the box take on the disease. Instead most turned their noses up to it as if it were a lump of feces served on a dinner plate. I can find no logical defense for this stance, as, with the best interests of their patients in mind, the MS establishment should have urged effective trials of the CCSVI hypothesis to be undertaken with great haste, to either prove or disprove CCSVI as quickly as possible. If proven right, the doubters could have quickly put a stake in the heart of CCSVI and moved on; if proven wrong, they would have ample reason to reassess their position and let the revolution begin. Either way, although the majority of evidence in favor of the hypothesis was and still is mostly anecdotal, the promise of a safe and effective new treatment and the potential of an entirely new way of looking at MS, developed by a reputable physician, should deserve serious scientific consideration.

On the flipside, some of the most fervent CCSVI advocates portray the hypothesis as a breakthrough cure for MS, a viewpoint that, while possible, simply isn't supported by the weight of the currently available evidence. A growing body of anecdotal reports certainly indicates that clearing blockages in the CNS associated veins of some MS patients provides relief of symptoms, but the degree of relief varies widely from patient to patient, and a signifiant number of patients experiences no relief whatsoever.

Although this lack of effectiveness of CCSVI treatment in some patients is of course disappointing, it really shouldn't be surprising, as we do know that MS presents itself very differently from patient to patient, and gets increasingly more difficult to treat the longer the duration of the disease. Different subpopulations of patients almost certainly have different disease triggers, and there's the distinct possibility that what we call Multiple Sclerosis isn't really one disease at all, but rather a collection of similar diseases that share symptomatic and diagnostic profiles. Vascular issues may play a large part in the disease of some patients, but a much smaller role, or no role at all, in the disease of others. There is still much to learn about CCSVI, and we don't yet even know the prevalence of the venous abnormalities collectively known as CCSVI in the healthy population. Stating anything about CCSVI, pro or con, with unequivocal certainty only sets one up to be proven wrong.

"MS is a vascular disease! Neurologists should step aside!" - It's easy to understand the frustration that many patients have with their neurologist, and neurology in general, over the CCSVI issue. Though one wouldn't expect neurologists en masse to wholly embrace the theory, the ham-fisted stonewalling experienced by many patients at the hands of their doctors has quite understandably left many angry and disgusted. Still, even in a best case scenario in which CCSVI proves to be a major key to unlocking the MS puzzle, neurologists would continue to have a major role in treating the disease. In such a rosy scenario, two possibilities present themselves: MS is a vascular disease with neurologic implications, or it is a neurologic disease with vascular implications. In either case, neurologists would remain a significant part of the picture.

Many of the interventional radiologists (the physicians who perform the CCSVI treatment) I've talked to describe themselves as medical plumbers. Their specialty is unblocking and fixing defective veins and arteries. They readily admit to having little or no knowledge of the neurologic implications of the venous abnormalities they're encountering in MS patients, they are simply attempting to fix what they see as broken vasculature and disrupted blood flow. Time and time again, the IRs doing CCSVI treatment have called on neurologists to join them in an interdisciplinary investigation of the hypothesis, for the very reason that the expertise possessed by neurologists is necessary to unravel all of the questions surrounding CCSVI.

As noted above, many MS patients are proving to be non-responders to CCSVI treatment. Their stories aren't heard much on MS forums or Facebook pages, and very few are making YouTube videos saying, "Look at me, I'm a CCSVI loser", but there are many MSers who have undergone venoplasty and experienced little or no benefit. I receive a steady stream of e-mails from some of these patients, perhaps because I too underwent the procedure but didn't experienced benefit (not that this has soured me on trying again, as I consider my procedure a "successful failure" (click here), and I expect to give it another go within the next few months).

Certainly, for patients who don't respond to CCSVI, neurologists will continue to play the primary role in treating their disease. Even in the case of CCSVI "hyper responders", in whom the treatment procedure works wonders, neurologists will be responsible for monitoring and treating the residual neurologic damage that will almost inevitably remain even if their disease has been eliminated. Unless caught in its earliest stages, MS does damage to nerve cells, which have little capacity for healing. Once damaged beyond a certain point, cells in the CNS do not regenerate, which is why those who suffer brain or spinal cord damage due to accidents or stroke rarely recover all of their lost abilities. MS patients with significant long-term mobility and/or cognitive issues would be left with serious neurologic deficits even if the MS disease process could be completely stopped by addressing their vascular issues. The advancing science of neuroprotective and neuroregenerative medicine falls squarely in the province of neurology. Therefore, like it or not, neurologists will remain a prominent part of the MS picture, regardless of the eventual success or failure of CCSVI.

"All trials done by researchers with connections to pharmaceutical companies should be disregarded" -On its face, this statement would seem to make sense due to the perceived conflict of interest of the researchers involved, and it's become the rallying cry against all published research with negative implications for CCSVI. The typical reaction sequence goes something like this: someone will post news of a research report critical of CCSVI on an MS forum, and within minutes other posters will report on the pharmaceutical company ties the researchers behind the report inevitably have. Case closed, the researchers were biased, and the trial results should be relegated to the trash heap.

The unfortunate truth, though, is that if all medical research done by investigators with ties to Big Pharma were to be disregarded, there would be practically no medical research left to ponder. The tragically dysfunctional medical research model that has evolved in the past several decades relies on Big Pharma to fund the vast majority of medical research trials. Furthermore, the tentacles of Big Pharma reach far and wide, their suckers touching almost all researchers and research facilities. The only entities completely untainted by pharmaceutical moneys are government and some academic facilities, both of which are woefully underfunded given our deficit laden government and the economic limitations of privately funded academia.

Given such a research milieu, it's almost impossible to find late stage medical research that is free from the taint of pharmaceutical financing. Almost all prominent researchers will have at some point in the careers been associated with pharmaceutical or medical device companies. This includes the heroes of CCSVI, the interventional radiologists. Just as there is stiff competition among pharmaceutical companies to woo neurologists to prescribe their immensely profitable drugs, medical device companies compete to get physicians to use their catheters, angioplasty balloons, and stents. Such are the realities of a medical industrial complex that feeds on the plight of patients. Let's not forget, too, that there is potentially a tremendous amount of money to be made treating CCSVI. The profit motive cuts both ways. We are already seeing the beginnings of aggressive marketing campaigns being conducted by CCSVI clinics in competition for patients, a development that will likely only increase as time goes on.

"Throw out your MS drugs; they're all snake oil and poison" - I'm no fan of Big Pharma and many of the products they produce. As for-profit public corporations, the big pharmaceutical companies are legally mandated to be beholden to their shareholders, not to the patients who take their products. Thus, the primary goal of any pharmaceutical company CEO is to increase their company's bottom line, a goal that is often at odds with that of finding cures, the development of which would effectively eliminate the consumer base of the company’s products. Multiple Sclerosis is now an $8 billion a year industry, and MS patients on disease modifying drugs have become indentured servants to the companies that produce MS medications.

That said, the current crop of MS drugs do increase the quality of life for a significant percentage of the patients taking them. No, they do not cure the disease. It is uncertain as to whether or not they even slow the progression of disease, as research can be found to support both sides of this issue (for "con" click here, for "pro" click here, here, and here). They do, however, cut down on the relapse rates of patients with relapsing remitting disease, in some cases to a dramatic degree. Since MS relapses can leave a patient incapacitated or days, weeks, or months, relief from them is no small achievement. This benefit does come at a potential price, as all of the MS drugs carry with them a wide range of side effects, and it seems the more effective a drug is, the more horrendous its potential side effect profile becomes. Still, many patients refuse to come off of these drugs despite the risk involved, due solely to the vast improvement they've seen in their quality of life as the result of having taken them.

Twenty years ago, MS was a "diagnose and adios" disease, one which physicians had almost no weapons to combat. For patients with RRMS, that picture has changed dramatically, even if the drugs now available are flawed, some deeply so. Progressive patients still have very little in the way of effective therapies, and their treatment options remained primarily those of basic symptom management.

MS is a terrible disease, a hateful and frightening thing that those who suffer from it, and those who love them, universally detest. My fondest desire is to see CCSVI fulfill its potential. But raising the bar to impossible heights, or making well-intentioned but reckless statements may only serve to impede the progress of CCSVI advocacy. Hope is a wonderful and vital commodity, but in matters so precious, it must be tempered by reason.

____________________________________________________________________________________

I've recently been working, along with several other MS bloggers, with a healthcare advocacy website called WEGO Health (click here). WEGO Health is conducting a study on people’s use of new technologies for health and they need your voice to understand the potential of technology to empower patients.

The survey will take about 10 minutes (you can stop anytime & come back later). All completed survey responses will be entered into a drawing to win an iPad, one of three iPod Touches or one of 200 iTunes gift cards. Everyone will receive a report on our survey findings.

This survey is only open until Friday, March 4, so if you'd like to help, please do so soon.

To take WEGO Health’s Health Technology Survey (click here)

CCSVI Video: Interview with Dr. Paolo Zamboni and Dr. Jack Burks

Sorry that things have been quiet here on Wheelchair Kamikaze for the last week or so, but I've been battling a bit of a bug. I hope you'll enjoy the following tasty tidbit of CCSVI information…

Here's another video sponsored by the CCSVI Alliance (click here), and edited by yours truly. It features an interview with the "father of CCSVI", Dr. Paolo Zamboni, and Dr. Jack Burks, an MS Neurologist who is the Medical Director of the Multiple Sclerosis Association of America. The interview was recorded on 01/17/11 in Miami Beach, Florida, at the International Symposium for Endovascular Therapy. Conducted by Sharon Richardson, the President of the CCSVI Alliance, the interview features Dr. Zamboni in person, and Dr. Burks joining via audio teleconference.

One of the biggest hurdles facing CCSVI researchers has been the reluctance of neurologists to get behind CCSVI trials, but this situation now seems to be shifting, and hopefully some much-needed interdisciplinary cooperation will be forthcoming. As is illustrated by the discussion in this video, CCSVI research is in its early infancy, and we've only scratched the surface on what needs to be learned. Momentum is building, though, and the next 6-12 months should bring much revealing data, as a host of trial information is scheduled to become available. Not soon enough for patients suffering from MS, I know, but we are getting there, slowly but surely.

And now, on to our featured presentation…

A Video Interview with My CCSVI Doctor

Image via Wikipedia

Sorry for the delay since my last post, but I've been a bit under the weather. Nothing serious, but as my fellow MSers know, just a touch of fever can really set MS symptoms afire. It's that whole heat sensitivity thing…

I'll be working on a new post in the next several days, but rather than leave everyone hanging, I thought I'd post this interview with the Interventional Radiologist who did my attempted CCSVI treatment, Dr. Salvatore Sclafani.

A quick recap for those who've discovered Wheelchair Kamikaze since my try at liberation: I underwent a catheter venogram procedure last March, which revealed that I do have a blockage in my right internal jugular vein, but, as with everything else about my disease, it's pretty strange. Unlike most other patients found to have the venous blockages associated with CCSVI, whose abnormalities occur inside of their veins, in the form of stenosis, valve malformation, or anomalous membranes, my blockage is caused by a muscle bundle outside of the vein pressing in on it, forcing it significantly closed. This blockage can't be addressed in the usual ways, with balloon venoplasty or with a stent, so further options are being explored.

I currently have tentative plans to undergo a second procedure with Dr. Sclafani sometime early in the New Year, to recheck my entire CNS venous system, as well as take another look at the blockage in my right internal jugular. Dr. Sclafani has learned much since I underwent my procedure nine months ago, as knowledge of CCSVI and how to treat it is evolving exponentially, almost by the day. This is why I've recommended in previous posts that those with milder symptom profiles and less aggressive disease should probably hold tight and wait 6 to 12 months before pursuing CCSVI treatment, since the procedures being done now are much more sophisticated than those done just a few months ago, and those done several months from now will be all the more refined. We'll also be discovering much more about the prevalence and impact of CCSVI in the coming months, as several trials start reporting initial results.

Unfortunately, my disease continues to progress rapidly, and I believe left unimpeded it will have me bedridden within the next 12 months, so I simply don't have the time to wait. Any port in a storm, as they say…

And so, without further ado, here's Dr. Sclafani, with a comprehensive assessment of the current state of CCSVI research and treatment, including an explanation of what CCSVI is, the methods used to treat it, the uncertainties surrounding the hypothesis, reasons for optimism, and the need for healthy skepticism and realistic expectations. BTW, I did not shoot this video…

CCSVI: Some Words of Caution

Image via Wikipedia

The subject of CCSVI (the vascular theory of MS) has proven to be incendiary, and has set the MS community ablaze. Initial studies into the hypothesis indicated substantial benefits could be gained by opening up the blocked veins in the neck and thorax of MS patients. These studies were soon backed up by an ever building wave of anecdotal patient reports of sometimes nearly miraculous improvements gained almost immediately after undergoing venoplasty, now known in the CCSVI universe as the Liberation Procedure.

In the wake of these reports, a tremendous amount of controversy has arisen, pitting MS societies and mainstream neurology against patients suddenly energized by hope, clamoring for access to a procedure they believe has a good chance to save them from the unrelenting ravages of the MS beast. Canada, which has one of the highest per capita MS rates in the world, has declined to even allow treatment studies of the liberation procedure to begin. Its single-payer health system refuses to recognize venoplasty as a potential treatment for MS, leaving Canadian MS patients with no options for treatment in their home country. The same situation holds true in most European countries. In the United States, the state of affairs is somewhat better, as an increasing number of physicians are offering the treatment to patients, although many health insurance companies won't cover it, and the cost of treatment is quite high. Additionally, waiting lists can extend for six months or more.

As a predictable result of this pent-up demand for treatment, a flourishing "medical tourism" industry has emerged around CCSVI, with clinics in Poland, Bulgaria, Costa Rica, Mexico, China, and India (and I'm sure I've forgotten a few) offering the procedure for a price, typically between $10,000-$20,000. It's been estimated that somewhere in the neighborhood of 2500 patients have visited these clinics, none of which have tracked the condition of their patients to any acceptable degree once the patients have departed for their home countries. Some of these patients have reported in at various sites on the Internet, but these patients probably represent less than 10% of the total patient population treated. Therefore, we have no good data on the effectiveness or safety of the treatments performed abroad.

The Liberation Procedure can take two forms: balloon angioplasty, in which tiny balloons are inserted into the veins and then expanded, thereby forcing open the veins, or stenting, a process involving the insertion of tiny mesh metal tubes into the veins, which when expanded prop the veins open. Often the two methods are used in conjunction, with patients receiving the balloon procedure in some veins, and stents in others. Both procedures carry the risk of clotting, although that risk is much amplified when stents are used. Because of this hazard, those who have undergone the Liberation Procedure are typically required to stay on a regimen of blood thinning anticoagulation medications for several weeks or months afterwards, necessitating the need for careful monitoring by qualified physicians to ensure the proper levels of medication are maintained. This aftercare can sometimes be hard to procure, as many physicians are reticent to treat patients for procedures that have been performed by foreign doctors and that they little understand. This problem has been especially prevalent in Canada, where the single payer health system has thus far refused to provide aftercare to patients that have gone overseas for "liberation".

In recent weeks, several troublesome (and in one case tragic) reports have begun to surface. Some patients returning from treatment in foreign clinics have experienced thrombosis (clotting) in their newly implanted stents, an extremely worrying condition that requires medical supervision (click here for article). In one truly horrifying episode, a young man who traveled to Costa Rica for treatment returned home to Canada, experienced thrombosis, and was turned away by local physicians when he sought their medical expertise. Ultimately, the patient returned to Costa Rica for treatment, and subsequently perished (click here for article). All of the patients in question had stents implanted in their jugular veins, which dramatically increases the chances of thrombosis when compared to balloon angioplasty, although that procedure too opens patients to potential problems with blood clots.

While the above incidents were transpiring, a conference on CCSVI was held at the annual ECTRIMS (European Committee for Treatment and Research in Multiple Sclerosis) in Gothenburg, Sweden. Many CCSVI research studies were presented, which are discussed in detail in the recently released article on Medscape.com (click here for article-you may be required to register at the site for access, a process which only takes a few minutes and is well worth the effort. Medscape is terrific resource for medical information). This article is quite long and offers an in-depth look at some very important research. It should be required reading for all patients interested in CCSVI.

The data presented at ECTRIMS was often in conflict, with some studies contradicting others, but the general consensus seems to be that while there is an identifiable correlation between CCSVI and MS, there is question as to whether CCSVI is the cause of MS. Rather, it may be a condition that is a result of the same disease process that causes the CNS damage seen in Multiple Sclerosis, or very possibly could contribute to the severity of the disease. It's quite possible that all of these scenarios may hold true, as MS differs so much from patient to patient that a variety of factors may result in its causation. In some patients CCSVI may play a major role in their MS, but in others it may play no role at all.

Given the above developments and wealth of new information, I feel compelled to offer the following words of caution. I know this message will not sit well with the most fervent CCSVI advocates, but I feel I would be remiss in not offering them.

While I am still a strong believer that CCSVI will prove to play a major role in unraveling the MS puzzle, I think that it is vital that patients use extreme discretion when choosing whether or not to undergo the Liberation Procedure, particularly if they must fly to far off destinations to procure treatment. According to one of the most experienced physicians performing the liberation procedure, Dr. Gary Siskin in Albany, New York, only about one third of patients treated receive dramatic improvements in their condition. Another third experienced minor benefit, and yet another third received no benefit at all. Furthermore, the rate of restenosis (veins closing back up) after balloon angioplasty is quite high, somewhere in the neighborhood of 50% within 12 months of treatment. These statistics alone should give patients some pause, as 66% of treated patients do not get the level of benefit they hoped for, and of those that do, 50% revert back to their previous condition, necessitating the need for additional procedures. This translates into 17% of patients who get liberated with the balloon method finding the lasting relief they sought.

The use of stents should be seriously questioned. In addition to the news reports above, Internet forums are revealing yet more patients suffering from stent thrombosis, and through this blog I've received numerous e-mails from other patients struggling with this problem. Stent thrombosis is only one of the potential hazards associated with the devices. The long-term failure rates of stents placed in the jugular veins is completely unknown. Most of the stents now being used were originally designed for use in thoracic arteries, where they are not subject to the nearly constant bending, twisting, and torque that they undergo when implanted in the extremely flexible human neck.

Data collected from two other patient populations that commonly receive venous stents (patients suffering from some cancers, and end-stage renal disease patients undergoing dialysis) is not especially encouraging. The failure rate of stents placed in dialysis patients has been found to be close to 50% after one year (click here for study). Although direct comparisons between disparate patient populations cannot be made, this data does provide reason for concern. Thus far, CCSVI patients treated with stents have not reported any instances of stent failure. However, the longest any of these patients have had stents implanted is only about 18 months, and the vast majority of patients fitted with stents have only received them in the last several months. I fervently hope that we do not start seeing a rash of stent failures in the months and years to come. The possibility can't be discounted, though, and only time will tell.

In conclusion, although CCSVI does hold tremendous hope for the future management of multiple sclerosis, we are presently in only the early infancy of investigation into the hypothesis and its relevance to the MS disease process, and of the practice of treating the condition with venoplasy. Beyond a doubt, future Liberation Procedures will bear little resemblance to those being done today, as new devices specifically designed for the task come on market, and the techniques and practices used to implement them are refined.

My heartfelt advice is that all those except the most desperate (and by that I mean patients with extremely aggressive disease who are quickly hurtling towards total disability) simply wait for 6 to 12 months before embarking on a quest for liberation. This will at least give some time for research to begin to catch up to patient expectations, and for physicians to better understand the best methods used to address the venous anomalies being found in MS patients.

I echo the warnings of virtually all of the most prominent physicians in the field, Dr. Zamboni included, that no patient resort to medical tourism in their quest for liberation. The risks of doing so are very real, particularly when the use of stents is involved. Balloon angioplasty is a much safer option, but the high incidence of restenosis means that many patients spending tens of thousands of dollars on treatment in foreign lands will find whatever gains they experienced lost, and will suffer not only from a return of their symptoms, but from broken hearts and broken bank accounts.

I fully understand the almost irresistible pull to get the disease taken care of NOW. I am close to being one of the desperate, if I'm not already there. This is why I chose to undergo a procedure this past March, which revealed a significant venous blockage but was unable to get it opened (mine is a very atypical case; the blockage is caused by a muscle outside of the vein pinching it almost closed). Hope is a powerful intoxicant, one that has been long absent for the vast majority of MSers. But we cannot and must not allow hope to eclipse reason. We all would like to see CCSVI advance as quickly as possible, but unfortunate events such as those recently reported will only provide fodder for those who would see the hypothesis relegated to the dustbin. Stay strong, friends, and act with extreme diligence.

Related articles

• Lack of MS treatment followup frustrates patient (cbc.ca)