The lives of MS patients may soon change dramatically based on a new medical discovery. According to new research, it appears that occlusions in the veins contribute to the disease process and pathology in MS. This newly described anomaly that has been demonstrated in the veins of individuals with MS is called chronic cerebrospinal venous insufficiency or CCSVI. This book offers a comprehensive look at this new research.
The Italian vascular expert and researcher Paolo Zamboni MD first recognized the significance of this finding and then advanced this medical discovery. As a professor of Vascular Surgery and Director of the Vascular Center at the University of Ferrara, Italy, as well as an internationally recognized vascular researcher, this physician is well-qualified to consider multiple sclerosis from a vascular perspective.
Dr. Zamboni also has a personal reason for wanting to fully understand this disease and find efficacious treatment; his own wife has multiple sclerosis.
My own interest in this new theory was inspired by the need for a new way to address my progressive MS; however, as an RN, my interest in new ideas always includes a critical evaluation of the associated peer-reviewed medical literature.
With this bias, I undertook the task of a complete review of the new CCSVI model, starting from learning about related research from vascular medicine and working through all of Dr. Zamboni’s research, his references, and pertinent related papers. I read hundreds of research papers over the course of a year. What I discovered as I investigated this model sparked my enthusiasm and formed the framework for this book and is presented in these pages.
Though CCSVI is a radical departure from the traditional view, which holds that MS is purely an autoimmune disease, Dr. Zamboni’s extensive years-long research offers a compelling case which suggests that a more accurate way of thinking about MS therapy should include evaluation and treatment of vascular anomalies as part of comprehensive MS patient care.
Treatment of venous malformations such as those Dr. Zamboni describes is currently available even though it will be some years before it will be clear exactly how the immune system and these newly revealed venous changes interact to cause MS. As a result of this lack of clarity, neurologists consider such treatment highly controversial even though vascular physicians consider angioplasty for similar problems routine.
The controversy finds its roots in the fact that neurologists deem current treatment of multiple sclerosis highly scientific and evidence-based even though such treatment does not cure MS. This book reviews this evidence base with a critical eye highlighting weaknesses in the traditional model and placing special emphasis on existing research that supports the idea that the new venous model is an important advancement in complete understanding of this disease.
In reality, there has always been evidence of a venous component to multiple sclerosis even though this extensive evidence had been largely ignored prior to this time. This fact lends added credence to the new research done in Italy.
Later chapters undertake in-depth review and discussion of the new research offered by the Italian research team headed by Dr. Zamboni. This is also balanced by discussion of weaknesses in the new theory as well as opposing research offered by critics. The result is a big picture view of how the new venous model may be seen taking into account the wider MS evidence base.
People evaluating this new research and treatment model will also presumably be interested in learning about treatment of venous problems with angioplasty. With this in mind, I have included information about angioplasty including issues that patients should be aware of as part of their consideration. Though vascular physicians such as interventional radiologists consider angioplasty routine, informed patients are more able to participate in meaningful discussion with these professionals.
The last part of the book is highlighted by stories of patients have been treated and can speak of their experience more than a year after treatment, including changes in their lives as a result of this new approach. My own story is included as I was treated early in 2009.
Finally, the book includes unique resources. These resources include information readers can take to local vascular doctors so that such physicians can participate in a trial and treat people with MS for CCSVI. There is also a detailed explanation of how to read the patient report if readers should be in a trial or see a physician that uses the Haacke imaging protocol, as well as ways to get involved with the activist patient community that is working to demand immediate, open-minded and thorough evaluation of this new idea should readers wish to participate.
One way people with MS and their advocates are making a difference is by supporting those entities established to raise funds for the extensive research that is needed to clarify how exactly CCSVI is involved with the MS process. Many different ways people can get involved in contributing to this effort are outlined in chapter 8, from small and simple to large. Together, MS patients and their advocates are making a difference. I am personally volunteering on the patient board of CCSVI Alliance a 501(3)(c) charity, which is a way to help raise funds for research of CCSVI.
I am also contributing 10 percent of my proceeds from this book directly to research of CCSVI through CCSVI Alliance.
This book is educational in nature and not to be taken as medical advice. It is intended to empower patients and to provide them with a background on the theory of CCSVI in MS so they may follow the research as it develops and to help prepare them for discussions with their own trusted medical advisors. The information included in this book is the author’s opinion, not the mainstream view, and may not apply to individual situations. Please consult your own medical professional for recommendations suitable for your situation.
Marie Rhodes is an RN who has been living with MS since 1993. She was the second person treated at Stanford for CCSVI and had angioplasty including a stent for venous stenosis in May of 2009. She is active on the internet as part of the grass roots movement to advance this research and raise awareness about this new work.
Chapter One
The Politics of Change
There are big changes taking place in the multiple sclerosis (MS) community. This disease, which doctors traditionally thought to be purely autoimmune, suddenly appears to have a significant vascular component. Research conducted in Italy by the vascular surgeon Paolo Zamboni, MD, suggests that the veins that lead from the brain and spinal cord in MS patients have significant blockages that vascular doctors could repair in a simple outpatient procedure. Some MS patients have had such procedures and highlights of their experiences are shared later in this chapter and in chapter 7.
Patients worldwide have embraced this new avenue of research and potential treatment with activist exuberance while neurologists look on in disbelief, dismayed as patients unexpectedly question their philosophy. The politics of medicine is changing.
“Politics” in this context refers to the ways in which people and institutions relate to each other, the dynamics and flavor of those interactions, the concerns regarding who has power, and the ways in which decisions influence the other players. In medicine there are many stakeholders ranging from pharmaceutical companies, to charitable societies, clinics, physicians of different specialties, research scientists and, of course, MS patients themselves. As research related to the vascular aspect of MS progresses, all of these stakeholders are finding that their traditional positions and the influence they used to wield have shifted.
Prior to the Italian research team’s discovery of the vascular defect, which they have labeled chronic cerebrospinal venous insufficiency (CCSVI), MS had been widely accepted as purely autoimmune. As a result, MS care was under the sole command of neurologists, and treatment was based on pharmaceutical approaches that suppress function of the immune system.
Naturally, this new way of looking at MS through a vascular lens has garnered skepticism among neurologists and pharmaceutical companies because they see the new idea as totally unrelated to the theory they had come to accept and which they felt was showing promise. They had come to believe that the autoimmune theory was unassailable.
It is not surprising that the first neurologists to express a public opinion about CCSVI took a purely defensive posture. A reporter interviewed a prominent MS neurologist researcher regarding media coverage of Dr. Zamboni’s research and quoted him as follows:
"I think there are going to be millions of dollars spent now to follow a hoax…" (Blackwell 2010).
This unfortunate comment polarized MS patients interested in CCSVI who felt it revealed a self-serving rejection of the new direction of research rather than the expected excitement about a potential breakthrough. Other neurology researchers cautioned that treatment of occlusions (blockages in the vein) should be halted until neurologists have conducted their own research and concluded that treatment that targets venous occlusion alters the course of multiple sclerosis. As one team of neurologists recommended in an article written in the journal Neurology:
“At present, invasive and potentially dangerous endovascular procedures as
therapy for patients with MS should be discouraged until such studies have been completed, analyzed, and debated in the scientific arena.”(Khan et al. 2010)
Such research as these neurologists are recommending would take 5-10 years. This unwillingness by some people in the MS field to accept Dr. Zamboni's findings as relevant to patients who may have these occlusions today ignores the fact that healthy circulation has value in its own right. It also neglects the fact that evaluation to check blood flow is currently available from vascular physicians......
Chapter 4
CCSVI Theory: MS as a Vascular Disease
When blood flows in a laminar way down the vein, meaning straight down without any swirls or eddies, the endothelium (the lining of the blood vessel) stays healthy. If there is something like a stenosis partially blocking the blood vessel, or an irregularity, then some of the blood refluxes and the flow becomes a chaotic, churning flow seeking a way out. When this happens, it causes a highly localized increase in venous pressure in the refluxing area, and this damages the function of the endothelium (Zamboni et al. 2008).
When there is either a blocked or a refluxing vein, the vein can’t do the job of draining the blood away neatly and efficiently, the endothelium changes, and the area that was supposed to be drained essentially gets sick, and it gets sick in a very predictable and specific way.
The first thing that happens is that the vein itself gets stretched out or varicose. This happens because veins, as different from arteries which are thick and strong because they have muscular walls to contend with the pulse, have very thin, weak walls with little muscle supporting them, so when the blood backs up in them and they become congested, then readily widen out.
This causes another kind of mischief. Most veins, with the exception of some of the cerebral veins, have valves in them, and these valves are critical to good venous return, so once the vein stretches out, the valve flaps are so far apart that they do not work well, which adds to the problem of venous return. With the valve flaps so far apart, the blood has nothing to hold it back so it slips back down the vein instead of moving toward the heart as it should.
This allows the congestion to build up further inside the vein and because of this there is more pressure in the vein than outside of it. This added pressure causes the stressed endothelium to allow the fluid to migrate out into the tissue. It moves through the vein wall and out into the adjacent extracellular spaces (the space between the cells). If the vein in question is in a leg, the most common site for these kinds of problems, the result is a puffy swollen ankle. If this goes on for some time, then not only will mere fluid from the circulation migrate out, but red blood cells will migrate out as well, followed by immune cells and that is bad news for the tissue in the area.
4.2.1 Iron in the Tissue and Immune System Activation
When red blood cells, which have iron in the form of hemoglobin in them, end up in the tissue instead of in the circulation, the immune system cleans it up aggressively because iron can trigger oxidative damage. Iron is important to many different cells and processes inside the body and for this reason the body’s iron stores are tightly regulated. Normally, iron is kept in the places where it belongs and removed by the body via the immune system when it is not (Chu et al. 2002; see also Quintana 2007).
When a person has iron that has been digested by the immune system, it is detectable using current techniques because it changes form into hemosiderin. It is the phagocytes that affect this change (Fischbach 1971; see also Chu et al. 2002). Hemosiderin deposits in the tissue are a sign of red blood cell leaking of one kind or another (Bourgouin et al. 1992) for example bleeding into the tissue such as in a hemmorhagic stroke, and subsequent phagocyte activity....
(this chapter goes on to discuss how this known information relates to CCSVI and potentially MS)
Each chapter has a plain language summery and editorial comment at the end to put the scientific concepts into perspective. The book also includes a glossary, index and detailed references including PubMed identification numbers so the reader can obtain the referenced papers to read themselves.