A group of Calgary neurologists has published a report on foreseeable complications faced by locals who have returned from going abroad and receiving trendy “liberation therapy” for multiple sclerosis. It is not clear whether the casefiles include the woman who was inadvertently liberated from the world by the treatment, but their contents sound troubling enough. “These five cases,” the authors note in their abstract, “represent the beginning of a wave of complications for which standardized care guidelines do not exist.”
They sound somewhat nervous, don’t they? It is almost as if they had not heeded the repeated reassurances of journalists and “liberation” enthusiasts that venous angioplasty and stent installation in major neck veins are routine procedures, of about as much clinical concern as having one’s shoe size measured. That tricky little distinction between veins and arteries turns out to be fairly important to the discussion: as an April letter in Clinical Neuroradiology pointed out, “Balloon dilatation and stent implantation have not primarily been developed for the venous system and are associated with a substantial risk for complications…with possible fatal outcomes.” [Emphasis mine]
Since the butcher’s bill is beginning to be drawn up, and not just in Calgary, it may be worth examining how well the “chronic cerebrospinal venous insufficiency” theory has fared over a full year of research. In April, SUNY Buffalo researcher Robert Zivadinov, a close colleague of CCSVI theorist Paolo Zamboni, delivered a controlled study of 500 patients that offered, at best, feeble confirmation of Zamboni’s original results. Zivadinov’s findings, as Colleague Anne Kingston pointed out at the time, could conceivably provide some comfort to both sides of the debate. But the one thing one could not possibly do with Zivadinov’s figures was to reconcile them with Zamboni’s original study, which claimed a perfectly sensitive, perfectly specific link between indicia of CCSVI and the presence of MS.
In the meantime, other results from preliminary studies of CCSVI and MS have been trickling out, to less fanfare. There is a cruel unrelentingness to them—a lamentable finality even to the titles of the articles. From Italy alone we have “No evidence of chronic cerebrospinal venous insufficiency at multiple sclerosis onset” (January); “Proposed chronic cerebrospinal venous insufficiency criteria do not predict multiple sclerosis risk or severity” (July); “Progressive multiple sclerosis is not associated with chronic cerebrospinal venous insufficiency” (last week).
A German team attracted some attention in January with a finding that “Intracranial venous pressure is normal in patients with multiple sclerosis”. A similar study from a VA hospital in Texas, using Zamboni’s own detection criteria to define the presence of CCSVI, was published earlier this month. The title: “No Cerebral or Cervical Venous Insufficiency in US Veterans With Multiple Sclerosis”. Meanwhile, the journal Neurology has a preprint from Greece which confirms the objectivity of the proposed CCSVI criteria—but also confirms the absence of any apparent link with MS. And for what it’s worth, a June study of animal models provides a smidgen of evidence against Zamboni’s speculation that vascular problems create autoimmune difficulties by causing localized deposits of iron to be left in the brain.
There is also the new study you might have read about which establishes that most of the gene markers statistically linked with MS are known to influence the immune system. For my money, that is actually an overhyped blow to the Zamboni hypothesis, in comparison with the lengthening train of papers finding no simple empirical connection between veins and MS at all. Most researchers agree that the CCSVI hypothesis is still worth following up with randomized controlled trials of larger size and longer duration. But they advocate this, not because there is any doubt that MS is fundamentally immunological, but because some far less radical variant of Zamboni’s idea might conceivably be, well, sort of true-ish. (See, for example, this note from neurologists in Erlangen: “…it certainly seems awkward to think of the complex disease MS solely as result of a simple venous outflow obstruction. Yet, the investigation of new vascular concepts as one variable in the pathophysiology of the autoimmune attack seems very worthwhile…”.)
Other researchers are frankly not so open to keeping up a chase that was, after all, set off by a study (Zamboni’s 100%-specific 100%-sensitive investigation) that almost certainly has to have been junk. The frustrations of a few scientists are discernible in the literature: one German group basically thumbed their noses at CCSVI by calling it the “perfect crime”—a supposed primary cause of MS that seems to leave no trace when sought in MS patients, using any means, by anyone but Zamboni or his very early supporters. Another comment in a senior journal asks whether CCSVI is “science fiction”. Either way, unfortunately, the premature enthusiasm for “liberation therapy” is cold inescapable fact.