This allocation was remarkable considering that many of the people who study and treat M.S. regard the theory as bunk. Dr. Robert Fox, medical director at the Mellen Center for Multiple Sclerosis at the Cleveland Clinic, says he sympathizes with patients pushing CCSVI research but thinks it offers false hope. “People without a scientific background,” he says, “often view all scientific papers with equal weight. Well, scientists don’t. I don’t know of a more prominent example where there’s been such profound pressure, driven by a nonmedical and nonscientific — though rightfully very self-motivated — constituency on what specific treatments should be explored with weak scientific basis.”

All seven of the studies the society is sponsoring are attempts to verify Zamboni’s discovery, which would entail finding CCSVI in a significantly greater percentage of people with M.S. than in healthy control subjects or in patients with other neurological disorders. Zamboni’s studies were small, and because he knew which subjects had M.S. and which did not, even he cautioned that “bias could be playing an important role” in his work. So far, evidence backing up his CCSVI theory has been scant: the largest study to date, led by Dr. Robert Zivandinov at the State University at Buffalo, found it at a higher rate in patients with M.S. (56 percent) than in healthy controls (23 percent) but also at a higher rate in patients with other neurological disorders, which some interpreted to mean that even if CCSVI were a significant abnormality, it is not M.S.-specific. Moreover, finding CCSVI at all is problematic. Researchers conducting studies in Israel, Italy, the Netherlands and Germany found no abnormal blood flow in M.S. subjects they examined. Whether a patient is said to have CCSVI can depend on a number of extremely variable factors, like the settings on the ultrasound machine, whether the patient is sitting up or lying down and what volume of blood flow the investigator pegs as “normal.” (Zamboni recently recommended a standard protocol.)

Many mainstream M.S. researchers share the opinion put forward by Florian Doepp of the Department of Neurology at Charité Hospital in Berlin after reviewing studies of CCSVI and M.S.: “I conclude there is no evidence for CCSVI in multiple sclerosis and no evidence to support” the surgical treatment for it.

Zamboni’s hypothesis contradicted substantial evidence supporting the autoimmune hypothesis, including the fact that more than 50 genes have been identified as associated with M.S., and every one involves the immune system and the most successful drugs against M.S. work on the immune system. Moreover, patients with Parkinson’s disease have abnormally high iron levels in their brains but don’t develop M.S., undercutting Zamboni’s idea that an iron backup in the brain leads to the disease.

Earlier this month, The Journal of Vascular and Interventional Radiology published a study concluding that using the CCSVI surgery in patients with M.S. “appears to be a safe procedure resulting in significant clinical improvement.” But the study did not rely on randomized or blinded data to protect against observer bias and the placebo effect. I showed the paper to J. A. Reekers, a Dutch professor of interventional radiology, the medical specialty that performs the treatment. “The scientific value of this paper is zero,” he told me. “M.S. complaints are very much related to external psychological factors.”

The author of the paper was Dr. David Hubbard, a neurologist who became interested in CCSVI after his son, Devin, found out he had M.S. in 2009. “Look, if not for my son I’d be on the other side of this,” Hubbard says. He knows that the only way purists of evidence-based medicine will be satisfied is a trial in which some people get the actual angioplasty and others undergo a sham operation. Such a trial would be expensive, but pressure from M.S. patients has made it possible: two such studies are now under way.

M.S. is a vexing disease: it progresses unpredictably both across and within patients, making a treatment’s effectiveness difficult to assess. Elena Zamboni and Adam Gottschalk still take Copaxone, so it is hard to know if it’s the vein-opening surgery or the drug keeping relapses at bay. But Devin hasn’t taken any of the disease-modifying M.S. drugs for years, Hubbard says, and not only has he had no relapses since the surgery, but his latest M.R.I. showed he has fewer brain lesions.