by Bnac Ccsvi Study

The Buffalo Neuroimaging Analysis Center Advisory Council prepared the following digest of the article, “Chronic cerebrospinal venous insufficiency in multiple sclerosis: diagnostic, pathogenetic, clinical and treatment perspectives”  for the benefit of MS patients and readers who are not neuroscientists. Dr. Robert Zivadinov is the lead author of this demyelinated diseases themed article published in the September 2011 edition of Expert Reviews: Neurotherapeutics, available by subscription.  Thank you for your interest in BNAC’s research.

Perspectives: CCSVI in MS

“Chronic cerebrospinal venous insufficiency in multiple sclerosis: diagnostic, pathogenetic, clinical and treatment perspectives” Published in Expert Reviews of Neurotherapeutics11(9), 1277–1294 (2011); Robert Zivadinov, Murali Ramanathan, Kresimir Dolic, Karen Marr, Yuval Karmon, Adnan H Siddiqui, Ralph HB Benedict and Bianca Weinstock-Guttman

The paper published in Expert Reviews is a broad and detailed examination of the current state of knowledge about CCSVI.

“Perspectives: CCSVI in MS” is intended as an abbreviated, guided tour of the original paper for those in the patient community with limited knowledge of medical terminology or without the time to study the entire original paper.

Excerpts from the original paper are indented and italicized; all other summaries and comments are those of the Advisory Council writers. Not included in this digest are tables, bulleted summaries, images, disclosures or references from the original paper. 

For complete detail please read the full paper

.  Names of the volunteer Advisory Council members who prepared this digest are listed at the end.

In the initial section on Historical perspective, the authors note that the underlying cause of MS remains undiscovered.  Going back to the early 20th century, researchers looked at the importance of abnormalities, obstruction of flow, and iron deposition in the veins that drain blood from the brain and spine back to the heart. Since 2008, Chronic Cerebrospinal Venous Insufficiency (CCSVI), a vascular condition reported by Dr. Zamboni, is being investigated by many different groups who report quite different results.

The paper summarizes the findings from BNAC's studies into CCSVI and contrasts their findings with research from other centers across the world.

Diagnostic techniques 

Color Doppler sonography

 is one of the ways to identify the presence of CCSVI in patients.  While Dr. Zamboni's original research  showed that 100% of the patients they studied met the venous haeomodynamic  criteria for CCSVI, other studies have reported widely varying levels of prevalence.

Q: Is there a standardized protocol for doing Doppler ultrasound testing for CCSVI?

A first attempt to define the standardized CCSVI scanning protocol was recently presented [27]. A more comprehensive document was recently developed at the first annual meeting of the International Society for the Neurovascular Disease in Bologna (Italy) in March 2011.

This consensus document was developed through participation of more than 40 international experts in Doppler imaging and should serve as a standardized screening tool for determining CCSVI status.

Doppler ultrasound has other disadvantages that are known:

• Need for special operator training


• The azygous vein cannot be directly examined


• Examinations are long, taking 1-2 hours


• Technical limits can prevent assessing all the criteria of the CCSVI protocol


• A patient's hydration can influence results

Q: Are all five of the CCSVI criteria equally valuable for diagnosing CCSVI?

The relative value of different CCSVI criteria is controversial. The CCSVI diagnosis combines functional and structural intra- and extra-cranial venous abnormalities in a single composite. Previous CV studies in MS [17,18,23,25] proposed that the extracranial venous anomalies are likely to be truncular venous malformations [48] characterized by intraluminal defects (such as flaps, webs, septums, membranes and malformed valves) or by extraluminal abnormalities represented by stenoses of the venous wall. In a recent study, 150 MS patients showed a significantly higher number of total and intraluminal structural and functional abnormalities on Doppler sonography compared with 63 healthy controls, while 46 progressive MS patients presented with significantly more extraluminal abnormalities than 104 nonprogressive MS patients [46]. These findings suggest that the majority of CCSVI pathology is confined to the intraluminal portion of the extracranial veins, which requires high-resolution B-mode imag- ing for visualization of these abnormalities. The visible ‘stenoses’ or extraluminal venous abnormalities probably only develop more frequently with progression of the disease [46].

The paper notes that determining reflux in deep cerebral veins (CCSVI criteria 2) has considerable variation because of individual patient physiological differences.

Q: Why is there such wide variation in the detected prevalence of CCSVI in MS patients?

BNAC has found that the detection of CCSVI by doppler ultrasound sonography is highly operator-dependent, indicating that standardized training is needed to achieve reproducibility of results.  The technicians who typically perform the procedure are not blinded from the patient leading to questions about the accuracy of testing performed.  Also, research at BNAC indicates that two of the five CCSVI criteria

 (2, 5) are less reproducible during repeat testing by the same operators than the other three criteria (1,3,4).  

One of the major limitations of all of the studies of diagnostic accuracy is the decision to categorize the criteria dichotomously. Zamboni et al. used =2 abnormal VH Doppler criteria as a cutoff for CCSVI diagnosis classification [17]. A potential problem of this approach is that the best fit of the criteria was biased toward characteristics of the studied population and based on the obtained results. The binary variable construct of the CCSVI diagnosis may contribute to explaining the major inconsistencies in findings between different studies.

Q:  Are there disadvantages in using Magnetic Resonance Venography (MRV) imaging for diagnosing CCSVI?

MRV imaging has advantages of being noninvasive, able to  depict intra- and extra-cranial venous systems in a short amount of time and with an ability to study flow and velocity.

Disadvantages are the lack of MRV dynamism in real time, lower resolution compared with Doppler sonography and CV (this is especially true for the detection of intraluminal structural abnormalities...)

Multiple studies at BNAC and elsewhere have reported that MRV imaging found no differences of detected CCSVI prevalence between groups with MS and those who were healthy.

The major explanation for the discrepancies between Doppler and MRV findings in various studies may be related to the fact that although head and neck veins are clearly displayed by MRV (especially the extraluminal venous abnormalities), the MRV cannot detect vessel wall or intraluminal venous abnormalities, in contrast to high-resolution Doppler sonography.

BNAC did find MRV complementary to use of Doppler ultrasound in subjects  who present with more extraluminal stenoses.

These findings suggest that MRV is useful in detecting IJV abnormalities, indicative of extraluminal stenoses, which are more frequent in progressive MS than in nonprogressive MS patients, or healthy individuals [47].

...the assessment of collateralization of the veins in the neck by MRV is more accurate than with Doppler sonography

Q:  What about Computerized Tomography Venography (CTV)?

The Prospective Randomized Endovascular Therapy in MS (PREMiSe) trial being done at Buffalo uses CTV to look for anomalies of the azygos vein compared with catheter venography.

No reliable diagnostic value of CTV was found for detection of venous abnormalities indicative of CCSVI.

Q:  Isn’t Catheter Venography (CV) the ‘gold standard’?

Catheter Venography  with contrast provides real-time information and allows measuring pressure in the veins.  However, there are a number of disadvantages.

• • Invasive


• • Definition of stenosis is subjective


• • Time consuming


• • Recognition of intraluminal abnormalities is difficult and requires experience and training


• • Malformed valves can be kept open by the catheter

... CV is merely lumenography providing little or no data on the vessel’s wall or its intraluminal structures. Therefore, in cases where only the intraluminal venous abnormalities are present, it is extremely difficult to measure the degree of stenosis by CV.

Use of a catheter that is pushed through malformations may keep open what would be shut when the catheter is not present.

Therefore, experience and proper training are needed for the recognition of abnormal valves or other pathologic intraluminal structures indicative of CCSVI.

Q: Does Intravascular Ultrasound (IVUS) provide better information?

There are advantages with IVUS:

• • Extravascular soft tissues can be penetrated [by ultrasound] from within the vein


• • Can assess blood vessels not easily accessible conventional ultrasound


• • Provides an image with a greater resolution of both the lumen and wall

In BNAC’s PREMiSe study, they found overlap between noninvasive doppler ultrasound results and those from use of invasive catheter venography with IVUS. BNAC’s results and recommendations are:

We found an acceptable overlap between Doppler sonography, IVUS and CV findings

Therefore, a multimodal approach is recommended to determine whether CCSVI exists and to what extent it is present in various healthy and disease groups, and MS sub- types. In addition, future multimodal approach studies need to establish whether the binary CCSVI diagnosis should be revised, with the introduction of more quantitative criteria that will provide the degree of extracranial venous structural and functional impairment

Origin and development of MS & CCSVI 

Q: How can blockages in the veins draining the central nervous system be associated with Multiple Sclerosis?

It's thought that the disrupted blood flow caused by venous blockages might contribute to the MS disease process in two ways: by depositing iron in the brain and spinal cord, and/or by reducing the amount of blood flow through the central nervous system.

Q: How may CCSVI affect the amount of iron found in the brains of multiple sclerosis patients?

It's been theorized that blockages in the veins draining the central nervous system may lead to blood refluxing back into the brain and spine, thereby disrupting the blood brain barrier (BBB) through a variety of mechanisms. The BBB normally prevents viruses, bacteria, and other toxic substances from passing from the bloodstream to the central nervous system, effectively forming a barrier protecting the brain and spine. The CCSVI hypothesis proposes that refluxing blood contributes to the breakdown of this barrier, and furthermore leads to the refluxing blood leaving behind iron deposits in the CNS.

It's long been observed that the brains of MS patients are abnormally high in iron, which is toxic to the tissues in the central nervous system. According to the CCSVI theory, iron deposits left behind by refluxing blood may be a primary cause of the damage seen in MS brains (as lesions), and could further contribute to or cause inflammation and activation of the immune response that is typically seen in MS patients.

However, there are other possible explanations for the iron deposits found in MS brains, as they may be caused by the debris left behind by damaged nervous system tissues, destroyed immune system cells, or hemorrhaging from damaged brain vessels. It is currently unclear whether iron deposition is a precursor to the MS disease process, or whether it plays a primary role in triggering inflammation and disease development.

Many uncertainties remain about the overall importance and contribution of iron deposition to the MS disease process, and if and how CCSVI contributes to this area of the MS puzzle.

Q: Can reduced blood flow caused by CCSVI result in Multiple Sclerosis?

Studies have shown that blood flow through the brains and spinal cords of MS patients is less than that of healthy subjects. It had been theorized that this might be due to inflammation in MS brains, or to decreased metabolic demand, but the CCSVI hypothesis proposes that the cause of this decreased blood flow (hypoperfusion) is the result of blockages in the veins draining the central nervous system.

The transfer of nutrients from the blood into the CNS is directly proportional to the rate of blood flow through the brain and spine. Therefore, reduced blood flow may significantly reduce the supply of brain nutrients and potentially result in damage to sensitive nervous system tissues.

A recent small study carried out by BNAC demonstrated that the majority of patients treated for CCSVI by balloon angioplasty experienced immediate temporary improvements in subjective complaints of fatigue and cognitive impairment. In another recent study, the reestablishment of cerebral venous return reduced chronic fatigue perception in a group of 31 MS patients with CCSVI who underwent the endovascular procedure, suggesting that fatigue could probably be associated with CCSVI. Though both studies were small and were not randomized, controlled, or blinded, they suggest that the impact of removing venous obstructions could increase blood flow through the CNS, thereby increasing the transfer of oxygen and nutrients into the brain, which may result in the reduction of complaints of fatigue and cognitive impairment.

Another small study demonstrated that hypoperfusion (reduced blood flow) through the brain of MS patients, but not in healthy controls, was associated with the presence and severity of CCSVI.

These findings, while provocative, need to be confirmed in larger, more comprehensive studies.

Q: Is CCSVI something we are born with, acquire, or both?

There are no answers yet; needs further study.

Q: Is CCSVI a consequence of MS or part of the disease development?  

Again, no answer yet.

Q: How does CCSVI fit into the current immune concept of MS, or does it not? 

It is strongly suggested by investigation at BNAC:

...that there is both reduced metabolism and anatomical reduction of venous vasculature in patients with MS that is strongly related to the presence and severity of CCSVI. 

There is a very large task ahead, even after BNAC completes their 1000 subject CTEVD study.

The interactions between the gene–environment MS risk factors and altered venous outflow in MS may present the scientific challenge in MS research – distinguishing between cause, consequence and association.

Recent 7-Tesla (7T) MRI studies show that a majority of MS lesions are associated with veins.

Whether occlusion of veins in the MS lesions may be related to blockage or reduced flow in the extracranial veins – that is, CCSVI – is currently unknown. Future 7T MRI studies should explore this topic.

We studied 59 MS patients and 33 healthy subjects. Subjects who presented with CCSVI presented with significantly decreased venous vasculature in the brain parenchyma. Findings suggest that there is both reduced metabolism and anatomical reduction of venous vasculature in patients with MS that is strongly related to the presence and severity of CCSVI.

Altered cerebrospinal fluid flow dynamics & CCSVI

Findings from our pilot study in 16 MS patients and eight healthy subjects suggest that the MS patients with CCSVI showed significantly lower net CSF flow, which was highly associated with the severity of CCSVI, compared with healthy controls.

Q: Is there a relationship between CCSVI & Epstein–Barr virus infection?

It has been suggested that EBV plays a role in the etiology of MS, but there is a high prevalence of previous EBV infection in the general population (virtually 100%).

Epstein–Barr virus has the ability to interfere with the immunological mechanisms that elicit both cellular and antibody autoimmune responses. One of the favored hypotheses for the role of EBV in the pathogenesis of MS is molecular mimicry between EBV and CNS antigens, leading to autoimmune attack on the CNS.

EBV can infect endothelial cells, causing venous thromboses and strictures of small vessels in the cranial and spinal venous drainage system. The mechanisms by which EBV infection may trigger venous thrombosis are not fully understood. Persistent EBV infection in the small vein vessel wall can directly promote a proinflammatory, procoagulant and proatherogenic environment.  

Q: Is there research into interaction between established MS risk factors and CCSVI?

In early 2009, our group started the Combined Transcranial and Extracranial Venous Doppler (CTEVD) study that investigated the prevalence of CCSVI in patients with MS, CIS, OND and in healthy subjects.

The study plans to enroll a target of 1000 subjects, among which will be 75 CIS and 550 MS patients with  various disease subtypes, and 300 healthy and 75 OND controls. In addition to CCSVI determination, all study subjects will receive an assessment for HLA-DR1501 status, vitamin D deficiency, immune responses to EBV and cigarette smoking. Therefore, CTEVD will be one of the first large studies in MS to assess interactions between the most established risk factors in a large cohort of MS patients at various disease stages, as well as in controls.

The interactions between the gene–environment MS risk factors and altered venous outflow in MS may present the scientific challenge in MS research – distinguishing between cause, consequence and association.

Q: What are the clinical, MRI & genetic perspectives of CCSVI & MS?

The pathogenetic mechanisms that would explain the reported associations between CCSVI and MS are yet to be determined.

In our large sample cross-sectional study, the prevalence of CCSVI was substantially higher in progressive MS than in nonprogressive MS patients [27] and there was a relationship between increased severity of CCSVI and increased disability [112]. However, in another smaller study, no association between CCSVI and clinical outcomes was identified [39]. It has also been shown that the presence of CCSVI was not significantly related to more severe lesion burden and brain atrophy in individual diagnostic subgroups or MS disease subtypes [113].

The lack of strong associations of CCSVI with [the gene] HLA-DRB1*1501 suggests that the role of the underlying associations of CCSVI in MS should be interpreted with caution [114].

In addition, recent genome-wide multicenter studies revealed multiple genes playing some role in MS, all of which except one being linked to the immune system [115]. Further studies should explore the association between CCSVI and genetic markers.

Therefore, although findings from the CTEVD study are consistent with an increased prevalence of CCSVI in MS (albeit with modest sensitivity/specificity) [27], they point against CCSVI having a primary causative role in the development of MS, as outlined in Table 1 [of the paper]. The higher prevalence of CCSVI in progressive MS patients may suggest that CCSVI may play a contributory role or be a consequence of disease progression [27,45]. The cause–effect relationship between CCSVI and MS should be further investigated. 

Q: What is known about the different endovascular treatments for CCSVI in patients with MS?

Balloon Angioplasty of veins (PTA) and stents

Endovascular treatment for CCSVI was introduced in an open-label study that evaluated the safety of percutaneous transluminal angioplasty (PTA) and its efficacy on clinical and MRI outcomes in 65 MS patients over an 18-month follow-up [18].

The authors [Zamboni et al] reported significant improvement in clinical, MRI and quality-of-life outcomes over the follow-up [18,84,116]. However, the interpretation of these findings is ambiguous given that this study was not blinded, not controlled and not randomized, and patients remained on standard disease-modifying treatment during the follow-up. The restenosis rate was elevated in the IJVs (47%), but much lower in the azygos vein (4%), suggesting the need for improved endovascular techniques. A logical alternative would be stent insertion; however, this option is potentially dangerous owing to the absence of dedicated devices of the proper size and length for the veins.

In collaboration with Italian investigators, the authors recently confirmed in the EVTMS study that PTA in expert hands is safe and well tolerated. No adverse events occurred and, at 1 year, the restenosis rate was 27%.

There is continuing research in the use of PTA.

To this end a pilot, double-blinded, placebo-controlled, randomized study (PREMISE) of 30 MS patients organized to preliminarily assess the safety and efficacy of PTA for venous stenoses in MS patients presenting with CCSVI over 1 year was initiated. A larger multicenter, double-blinded, randomized, placebo-controlled trial, entitled BRAin VEnous DRainage Exploited Against MS (BRAVE DREAMS), will assess the safety and efficacy of PTA treatment for CCSVI over 1 year.

... use of stents should be avoided until proper devices are developed, tested and validated.

Given the potential postintervention short- and long-term risk related to the use of stenting [23,117,119], and medium to high risk for restenosis after PTA [18,82], CCSVI intervention should be restricted to blinded, randomized and controlled clinical trials that will establish the safety and efficacy of these procedures.

Q: What are the authors’ Conclusions, Comments?

CCSVI and its possible relationship with MS 

• • Chronic cerebrospinal venous insufficiency (CCSVI) is a condition that has been described in MS patients with high frequency.

• • CCSVI is characterized by the impaired brain venous drainage due to outflow obstruction in the extracranial venous system mostly related to anomalies in the internal jugular (IJV) and azygos veins.

Diagnosing CCSVI

• • Multimodal comparison studies suggest that Doppler sonography in properly trained hands could be the most reliable and cost-effective diagnostic and screening noninvasive tool for CCSVI.

• • Given that a growing number of reports refute the association of CCSVI with MS, one or more diagnostic gold standards need to be determined and standardized diagnostic and research interpretation guidelines validated.

Mechanisms of CCSVI and how they relate to established risk factors  

• • The possible origin of these abnormalities could be congenital [48], aging-dependent [127] or a possible consequence of an inflammatory process. Further research is needed to determine whether these anomalies represent a pathological condition or a physiological variation.
  

• • Mounting evidence suggests that a number of inflammatory and neurodegenerative central nervous system (CNS) diseases may be related to venous anomalies [125,126].

• • Emerging evidence is pointing against CCSVI having a primary causative role in the development of MS; however, higher prevalence of CCSVI in progressive MS patients may suggest that CCSVI may play a contributory role or be a consequence of disease progression.

• • Chronic cerebrospinal venous insufficiency is a controversial area in MS research and it is important to critically assess the role of CCSVI and its effect on the body so that the implications, if any, for the treatment and prevention of MS can be determined.  

Treatment  

• • More than 12,000 compassionate procedures around the globe have been performed to improve venous return in MS patients [118].

• • Although there is no scientific centralized registry that would capture self-reports of all patients who underwent the endovascular treatment for CCSVI, their personal descriptions range from ‘miracles’ to ‘worsening’ of their MS symptomatology postprocedure.

• • Safety complications are only anecdotally reported on the internet and probably largely underestimated.

• • Potential usefulness of endovascular treatment for CCSVI in patients with MS is unknown and should be established in future blinded, randomized, controlled clinical trials that will need to assess the benefits of endovascular interventions according to established clinical and MRI treatment outcomes. 
  

• • Only safe and ethical approaches should be encouraged in designing new clinical trials that will investigate this important part of the puzzle. If such trials establish an initial benefit for endovascular therapy, then properly powered Phase III clinical trials should be conducted to prove whether this type of treatment can be made widely available. Until these steps are accomplished, there is no role for the endovascular treatment of CCSVI in MS patients outside of approved clinical trials.

Summary conclusions and commentary  

• • More evidence is needed to establish the association of CCSVI and MS.

• • Intensive research toward better understanding of the venous system and the MS disease process should be continued.

• • It is essential that the CCSVI theory be investigated further and in more depth…current evidence for the association between CCSVI and MS justifies performance of blinded, randomized, controlled clinical trials that will assess the benefits of endovascular interventions according to established clinical, MRI and quality-of-life treatment outcomes.  

• • Of particular importance is the need to define the most accurate screening and diagnostic tools for CCSVI and for the follow-up of those individuals who have undergone endovascular treatment. Preliminary comparison studies suggest that Doppler sonography in properly trained hands could become the most reliable, cost effective and noninvasive diagnostic and screening tool for CCSVI.

We hope that readers have learned more about the current information on  CCSVI as reviewed by a group of researchers who are continuing to actively seek new knowledge about CCSVI & MS.

BNAC Advisory Council - Patient Education Committee members who worked on Perspectives: CCSVI & MS:

Michelle Brown

Larry Nolan

Marc Stecker

Craig Walters

September 14, 2011

                                             Buffalo Neuroimaging Analysis Center

                                                               A division of

                 Univ. at Buffalo Department of Neurology:The Jacobs Neurological Institute 

                                                         2011-12 Advisory Council 

                                                          Tracie Jacquemin, Chair

Michelle Brown                                  Larry Nolan                        Trevor Tucker, PhD

Larry Montani                                    Marc Stecker                      Craig Walters

Ex officio

Robert Zivadinov, MD, PhD, FAA  BNAC Director

Linda Safran, CFRE, Director of Development

Eric Alcott, Sr. Associate Dean of Medical Development & Alumni Relations

Michelle Brown, a magazine publisher, was diagnosed with MS in 1998. After 8 years of a benign course, she developed secondary progressive MS, and her mobility deteriorated within 2 years to leave her wheelchair-bound. She is an alumna of SUNY Albany with a degree in psychology and did postgraduate work in marketing at the University of Connecticut. Michelle read about CCSVI in early 2009 and became the first patient treated on the East Coast in December 2009. Shortly afterwards, she founded and incorporated the CCSVI Alliance.  Michelle commutes by train to her New York City office several days each week where she works full-time. She resides in Greenwich, CT, with her husband, two daughters.

Tracie Jacquemin is chair of the BNAC Advisory Council.  She lives in McLean, Virginia with her husband and their three daughters. In addition to her work with BNAC, Tracie is a volunteer with the Kenya Education Fund and the Greater Washington Suzuki Association of the Greater Washington Area. An alumna of Duke University where she received her BA, she also earned an MBA from Vanderbilt University and worked in banking and commercial real estate for ten years. After being diagnosed with multiple sclerosis twenty years ago, Tracie became a certified as Montessori teacher and worked as an educator for many years.

Larry Montani is Managing Director of Niacet Corporation, a specialty chemical manufacturer based in Niagara Falls, NY. Born in Milton, MA, Larry earned a Bachelors degree in Civil Engineering from Merrimack College and a Masters in Business Administration from the University at Buffalo.  He and his wife and children have lived in Western New York for 27 years where Larry is active in the community, serving on the boards of trustees of Niagara University, the Nichols School, and the Foundation of the Roman Catholic Diocese of Buffalo. Larry served as chair of the National MS Society Upstate NY Chapter 2004 Dinner of Champions and was recognized as a 2009 Community Champion. His work to advance the understanding of MS is inspired by three siblings with MS, one of whom is now deceased.

Larry Nolan and his wife, live in University City, Missouri. After 37 years as a software developer and product manager in the mechanical CAD/CAM/CAE industry, he is now a volunteer for The Nature Conservancy in Missouri. He has a B.Sc. in Applied Mathematics from Missouri University of Science & Technology, M.Sc. in Computer Science from Washington University in St. Louis. Larry’s wife was diagnosed with RRMS in 2008 after her neurologist suspected this diagnosis in 2007.

Marc Stecker is the writer of the award-winning medical blog, "Wheelchair Kamikaze", one of the first sites on the Internet to feature information on Dr. Zamboni and the CCSVI hypothesis. Diagnosed with PPMS in 2003, Marc had a 20-year career in the television production industry before being forced to retire due to disability in 2007. He lives in New York City with his wife and spends much of his time writing about life with chronic illness, as well as working on photographs and videos that he takes with his wheelchair-mounted camera.

Trevor Tucker has a PhD in Electronics Engineering from the University of British Columbia He is founder and President of Tactical Technologies Inc, a software simulation company in Ottawa, Canada.  He is married, has a son, a daughter, and four grandsons.  Trevor’s son was diagnosed with MS in 1998.  He is an advocate of a multi-disciplinary approach to the solution to Multiple Sclerosis and has recently applied the physics of fluid dynamics to addressing the association of obstructed veins to MS. 

Craig Walters  From Connecticut, and an avid sailboat racer for fifty years, Craig began designing and building sailboats at age 12. He earned a BSBA degree from Bucknell University, served as an Officer in the Army Corps of Engineers and was a yacht designer with Morgan Yachts, Sparkman & Stephens and firms of his own in Florida and Connecticut. From his interests in protecting the marine environment, Craig developed a series of electric and hybrid powered pleasure boats in the 1990’s and has written and lectured about yacht design. Craig was diagnosed with RRMS in 1970, now classified as Benign MS, and also has CCSVI. He and his wife now live in Southwest Florida where they recently retired.                                                                                                                                                                                                 9/14/11

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