Original article link: http://msandccsvi.com/a-review-of-%E2%80%9Cintegrating-ccsvi-and-cns-autoimmunity-in-a-disease-model-for-ms%E2%80%9D/
A review of “Integrating CCSVI and CNS autoimmunity in a disease model for MS”, A.F. Embry, Direct-MS, Calgary AL, Canada; International Angiology, 2010, April, 29:93-4.
In this article, Embry reviews initial studies regarding CCSVI from Zamboni, Simka, Khan et al, University of Buffalo, Lee and Lucchinetti in order to discuss the current model of Multiple Sclerosis (MS) in the professional community. Presently, MS is characterized as a cell-mediated, autoimmune disease, based on genetic, immunological, experimental and epidemiological data per MacFarland and Martin (National Immunology, 2007). However, this theory has been recently challenged by the newly defined condition of Chronic Cerebrospinal Venous Insufficiency (CCSVI). CCSVI theory supposes that “venous blockages lead to reflux of blood into the brain which, in turn, lead to upregulation of adhesion molecules on the blood brain barrier (BBB), iron deposition, subsequent inflammation, and breeches of the BBB” (per Zamboni and Simka). This sequence of blood products into the central nervous system (CNS) initiates inflammation and neurodegeneration, which, consequently, cause the neurological effects which exemplify MS.
Embry discusses various studies in reference to Zamboni’s research and findings as well as replication of his work with Dr. Robert Zivadonov and Dr. Bianca Weinstock-Guttman at University of Buffalo, NY. But, prior to discussing the work at Buffalo, Embry reviews the findings of Dr. Byung-Boong Lee at Georgetown University. Dr. Lee has found that CCSVI venous malformations are of congenital origin, meaning that these venous problems are not the result of post-birth physical deterioration or environmental causes or trauma. This key point is crucial for determining how physicians and scientists will deal with CCSVI.
Then, Embry moves on to the results of the University of Buffalo study. In reviewing the results of Phase I of the Buffalo study (total 1,600 subjects—500 in phase I), the following data was listed:
56% of persons with MS in the study had CCSVI
22% of healthy control participants had CCSVI
38% of those with an initial demyelinating event had CCSVI (not yet diagnosed with MS)
80% of those with more advanced MS had CCSVI
Embry describes that since 22% of healthy control subjects had CCSVI and 56% of persons with MS (not 100%) have CCSVI, this study demonstrates that CCSVI alone does not cause MS. In addition, these results indicate that the higher the level of disability in MS patients, the higher the CCSVI involvement. This correlation indicates that patients with both MS and CCSVI have the chance of progressing to a higher level of disability than MS patients who do not have CCSVI.
The results from the Buffalo Phase I study indicate that neither the autoimmune or CCSVI model of MS alone is sufficient to define the disease process.
One proposed model that could fit allows for MS as a CNS autoimmune disease which is exacerbated by the presence of CCSVI. This proposed model fits the data from the Buffalo Study, thus far, and allows the reader to believe that CCSVI is a real part of the MS disease process. Due to the result of CCSVI on MS disease progression, detection and treatment are extremely important. According to Embry, “scans to determine the presence and nature of venous problems will be just as important as standard MRI scans when it comes to diagnosing and designing treatment regimens for patients”.
Article review by: Kristen Cuenca, RNC, MSN, Case Manager, WorldMed Assist