I have been following the story of chronic cerebrospinal venous insufficiency (CCSVI) as a new hypothesis for the cause of multiple sclerosis (MS). The idea comes from an Italian vascular surgeon, Dr. Zamboni, who claims that blockage of the veins that drain the brain are the primary cause of MS. His initial study on this question found 100% of MS patients he studied had this blockage.

There are numerous problems with this hypothesis, however. First, we have decades of research indicating that MS is an autoimmune disease. The immune system attacks the central nervous system, causing flares of inflammatory plaques that damage myelin (the insulation around axons) and disrupts the flow of signals. While we don’t understand everything about what causes the disease, what we do know does not square well with the notion that it is all being driven by venous blockage.

Zamboni’s idea has been met with appropriate skepticism by the neurological community, but at the same time it has been widely studied in just the few years since it was proposed. The community is doing its due diligence and not rejecting the idea out of hand. The studies coming in so far have been largely negative. No one has replicated Zamboni’s original results. Various studies just looking at the correlation between venous blockage and MS have had varied results, but nothing approaching Zamboni’s 100%. Some studies found no correlation, others a possible small correlation.

This left open the possibility that, while not a primary cause of MS, there may be a pathological association between MS and CCSVI. Perhaps, for example, MS inflammation causes CCSVI, which can then contribute to MS severity. So while Zamboni may not have revolutionized our understanding of MS, he may have found a contributing factor.

Even this lesser claim for CCSVI, however, is not fairing well. A recent  unblinded study looking at patients who went for the liberation procedure to open up the cerebral veins found no benefit. In fact, even in cases where the veins clot off completely there is no worsening of MS. Similarly a rat study in which rats with an experimental model of MS had their jugular veins ligated did not suffer any worsening of their MS compared to rats without the ligation.

Now we have yet another piece of evidence that indicates that CCSVI does not even contribute to MS severity. The researchers studied subjects with MS and healthy controls. First they established who had CCSVI, and they found:

The diagnosis of CCSVI was assigned by using specific color Doppler ultrasonographic criteria. Cerebral blood volume (CBV), cerebral blood flow (CBF), and mean transit time were assessed with dynamic susceptibility contrast material–enhanced magnetic resonance imaging in normal-appearing white matter (NAWM) in 39 patients with MS. Of these, 25 had CCSVI and 14 did not. Twenty-six healthy control subjects were also evaluated, and of these, 14 had CCSVI and 12 did not.

That’s 64% of MS patients in the study with CCSVI, and 53% of healthy controls.  This is similar to other studies in that there may be a slightly higher incidence of CCSVI in MS, but not by much. They then looked at the effect of CCSVI on brain hemodynamics and on MS severity, and concluded:

The data support a role of CCSVI in cerebral hemodynamic changes, such as a decrease of CBV and CBF, regardless of the presence of MS. CCSVI had no effect on neurologic function and disability progression in patients with MS.

So – there may be a slight correlation between MS and CCSVI. CCSVI, whether in MS or healthy controls, does have an effect on blood flow in the brain. But – there does not appear to be any effect on MS severity.

This is just one study, and it is relatively small, so it’s not the last word on this score. However, it adds to the growing scientific literature on the questions of CCSVI showing that it is, at best, a small phenomenon in MS, it does not appear to contribute to MS severity, and treating it has no benefit.

In other words – CCSVI in MS appears to be a dead end.

In a perfect world the scientific evidence would be the final word and we would collectively move on. However, in addition to watching a new hypothesis go through the stages of scientific research, we are also watching a popular conspiracy theory evolve from this hypothesis. There is a populist pro-CCSVI movement, driven largely by MS patients who are not responding to standard treatment and are desperate for an alternative.  It is distressing how quickly they turned on the neurological community, accused them of  a conspiracy, of being in bed with (of course) “Big Pharma”, and of suppressing the truth.

There are many clinics now offering the liberation procedure, without any evidence that it helps or even that it does not cause net harm. There is a CCSVI Alliance to promote this diagnosis and its treatment. There is political pressure to fund more and more research into the treatment of CCSVI, despite its poor showing in existing research. There is a larger and larger disconnect between the scientific community and the pro-CCSVI community as the data comes in increasingly negative.

CCSVI is taking on a life of its own, ahead of, and in fact despite, the scientific evidence. There is a developing infrastructure and belief system that will not be easily dismantled. My fear and suspicion is that, once the scientific evidence against CCSVI is solid and complete enough that it is truly dead as a scientific hypothesis, it will live on in the fringe. It will become yet another “alternative” treatment with its devoted adherents.

If history is any guide, it’s possible it will survive for decades. Twenty years from now there will still be CCSVI institutions and practitioners exploiting MS patients with the false hope of the liberation procedure. They will be endlessly calling for more research to finally prove their claims correct, while finding reasons to dismiss existing negative research, and rewriting history to suit their conspiracy narrative. Meanwhile the memory of CCSVI will have mostly faded from mainstream medicine, and a new generation of neurologists will not even know what it is.

There are many examples of treatments that have followed a similar course: psychomotor patterning, chelation therapy for heart disease, laetrile, bee sting therapy for MS, facilitated communication, repressed memory syndrome, and others – all decades old. There are still older therapies that linger to a greater or lesser degree, and some that are even experiencing a resurgence: magnetic therapy, radio frequency therapy, energy medicine, homeopathy, iridology, and even classics like phrenology and blood letting still have their fringe adherents. These are all ideas discarded by science a century ago or longer.

It already seems too late to nip the CCSVI machine in the bud. Scientists are doing all they can – researching the idea despite their skepticism, and far more than the idea merits, partly because of due diligence and partly because of the popular support for the hypothesis. Evidence will affect the attitude of the scientific community. It generally has little effect on believers and proponents.

Perhaps much of the fate of CCSVI will rest with Zamboni himself. If at some point he recants his claims in light of the scientific evidence, it may be enough to suck the wind out of the sails of CCSVI. The question is – will he have the courage to say that his idea was simply proven wrong by diligent scientific evidence, or will he cling to CCSVI as his legacy and become a cult hero to the medical fringe?