The discovery of a cure for MS will not be attributable to a single medical breakthrough but a series of medical discoveries and innovations leading to the cure. This process will involve biochemists and vascular researchers; physicists and radiologists; engineers and neurosurgeons, immunologists and geneticists among many other scientific disciplines. This is not to discard the new theory of a vascular disease connection. But that is only the snowball that got the avalanche moving down the slope. The theory that a simple dilation of the jugular veins can achieve a cure for MS oversimplifies the explanation of the disease pathways and ultimately obscures therapeutic objectives. Since it was proposed three years ago, it has also politicized a specific disease like never before. Anyone looking at the empirical evidence demonstrated by the growing number of MS patients who are commonly affected once the retrograde blood flow pressure on the brain is relieved by expanding the occluded jugular veins will quickly agree that Zamboni’s hypothesis is more or less correct; that an equalization of the outflow of blood from the CNS to the heart muscle is essential to reducing the presenting symptoms of MS. But the surgical act of neck vein dilation by itself will not come close to providing the cure. Once the vascular pressures are balanced, only a correlation between a vascular event and the disease itself has been demonstrated. The occluded neck veins do not explain the autoimmune trigger that causes the disease. Connecting those dots via the clinical findings from the effect of autologous cells transplanted to the MS brain goes a long way toward the explanation, but again does not identify the trigger. In individuals predisposed to MS, whatever prompts the autoimmune response, inevitable and irreparable damage to the myelin and the interlaced axonal matrix occurs through the pattern of the disease. In multiple clinical trials, suppression of the disease event cascade has been demonstrated with the introduction of Mesenchymal stromal cells (MSCs) to the diseased CNS. Once these cells are introduced, the resultant biochemical event sequence has been observed, biochemically identified, measured and described in several important trials. Where the retrograde pressures caused by the stenotic vessels reflux and deposit deoxygenated and iron-rich hemoglobin on the myelin covering of the CNS, MSCs respond by inducing suppression of various immune cell populations and inhibit white blood cells from evaluating the sites of insult and erythrocyte extravasations. But it’s still not known why only some people get MS since the same diseased pathology and internal biochemical conditions exist in human populations that never exhibit the autoimmune response. The good news is that it may not have to be known for the time being. The therapeutic benefits of MSC transplantation have been clinically observed in human subjects. The stem cells, once introduced to the CNS, create the same internal environment where the MS patient’s over-aggressive immune system is suppressed. These stem cells, if present in sufficient numbers, then locate themselves to the areas of disease to replace the damaged nerve and tissue cells. In therapeutic trials on human subjects, the recovery of neurologic deficits in many patients has been remarkably rapid and complete. For MS patients transplanted with stem cells that suppress the disease syndrome and go on to regenerate all tissue and neurons that have been damaged by the disease, the obvious question is then whether the diseased neck veins need to be treated at all? The answer may lie in the MS patient’s abnormal vein pathology. By establishing a diagnosis of Chronic Cerebrospinal Venal Insufficiency, a disease condition has been noted. Furthermore a clear correlation has been established between the pathology and the disease through statistical and observational evaluation. In some southern countries where MS does not exist in numbers in the general population, CCSVI in the jugulars has been noted and corrected as treatment for some types of optic neuritis, a symptomatic indicator for MS (and another autoimmune disorder). Once the neck veins are widened, the symptoms of optic neuritis are alleviated. Minimally invasive procedures to treat optic neuritis (and other specific conditions) by way of jugular venoplasty have been going on in some countries for the decade before Zamboni publicized his liberation theory to the world in 2009. To several groups of neurosurgeons in India, Central America, and South America, Zamboni’s theory was no surprise; in fact it made perfect sense. This therapeutic treatment modality for an autoimmune disorder that is not considered to be MS, yet has some of the same presenting symptoms of MS, is further confirmation of a vascular connection to the disease. Therefore the pathology of the neck veins in MS patients cannot be ignored. And if this statement is accepted as true, then there are many more questions that fall into line. The greater problem is what to make of the vein dilation therapy as it’s currently being practiced on MS patients by IRs in clinics around the world? While MS patients in the thousands fly hither and yon to receive the ‘liberation therapy’ on an outpatient basis claiming it is their right to do so, are they really receiving the most effective therapy for their disease? Or is only one part of the ‘bandwidth’ being treated in a general disease condition that requires a ‘spectrum’ approach to treatment? To start with, the high rate of thrombosis and restenosis that occurs immediately post-procedure indicates that it should never be considered as an outpatient procedure. Yet up until now the clear need to monitor patients post-procedure to avoid risk of complications has not been a focus of either therapeutic practice or of the research, and at least therapeutically, has not been seen as necessary by the practitioners. This avoidance of post-procedure aftercare and lack of follow-up with MS patients just having undergone venoplasty is remarkably at odds with the evidence and consistent with the financial biases inherent in the current system of management of CCSVI. And what happens when an aftercare protocol that supports post-procedure wound healing in the newly remodelled jugular veins is ignored by the IRs writing the current Trial Protocols? If the NL Study findings are repeated in the larger New York Trial currently funded by Saskatchewan and other levels of Canadian governments, the patient outcomes will quite predictably, be precisely the same (within the same statistical margins for error). The conclusion of ANY trial that ignores the clear need to keep the patient in the hospital, in a quiet and supine position, and monitor the jugular veins for complications after the liberation procedure for a period of days, and be prepared to re-treat if necessary, is doomed to repeat the NL Study findings. Unfortunately the ‘liberation therapy’ will not be approved; the MS community will dig their heels in on one side and the medical establishment on the other and the politics of MS treatment will continue.For more information please visit