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Dr. Marian Simka, who, working out of Poland, has perhaps performed more CCSVI liberation procedures than any other interventional radiologist in the world, has released the following summary of a soon-to-be released research paper. Its findings are dramatic, and have already provoked much discussion on CCSVI sites around the web and on Facebook.
Dr. Simka's summary:
"CORRELATION OF LOCALIZATION AND SEVERITY OF EXTRACRANIAL VENOUS LESIONS WITH CLINICAL STATUS OF MULTIPLE SCLEROSIS" Simka M, Ludyga T, Kazibudzki M, Latacz P, Świerad M, Piegza J EUROMEDIC Specialist Clinics, Department of Vascular & Endovascular Surgery, Katowice; Poland.
ABSTRACT: Background. Chronic cerebrospinal venous insufficiency is suspected to play a role in pathogenesis of multiple sclerosis.
Objective. Assessment of the correlations between patterns of venous lesions and clinical characteristics of multiple sclerosis.
Methods. Localization and degree of venous blockages in multiple sclerosis 381 patients were evaluated using catheter venography. Analysis of clinical severity included: Multiple Sclerosis Impact Scale-29 (MSIS-29), chronic fatigue and heat intolerance assessment.
Results. Venous blockages were found in 97.1% of the patients. Abnormalities were more severe in older patients. No correlation existed between duration of the disease and severity of venous pathologies. Patients with younger age at onset of multiple sclerosis presented with milder venous lesions. Significant correlations existed between severity and localization of venous lesions and clinical burden in terms of MSIS-29 and chronic fatigue scores, but not of heat intolerance.
Conclusion. Prevalence of chronic cerebrospinal venous insufficiency among multiple sclerosis patients is very high. Indirect data analysis indicated that venous abnormalities are probably congenital, slowly progress, but are unlikely to be caused by multiple sclerosis. Their severity and localization significantly modify clinical course of this disease. However, they are not likely to directly trigger multiple sclerosis, but there may be another factor initiating the disease."
The above summary is short, but packed with tantalizing nuggets of information. Of course, the first item that leaps off the page is the finding that 97.1% of MS patients have venous blockages. Needless to say, this is a very compelling number, and begs for a comparison with the commonality of such blockages in healthy subjects. Unfortunately, to my knowledge no study using catheter venography on healthy patients has yet been done, so this data is simply not available. We can assume that the incidence of venous abnormalities in the general population would be much less than 97.1%, however, venous anatomy has been so little studied that I don't think such a statement can be made with complete confidence. Hopefully, the full paper will expound on this subject.
It's also interesting that Dr. Simka concludes that CCSVI venous abnormalities are probably congenital, but slowly progress. This conclusion would seem to be supported by his a summary of results, which found that younger patients presented with milder lesions, and older patients with more severe ones. I'm not sure of the biological mechanism that would lead to congenital deformations slowly getting worse with age. I had assumed that malformations present at birth would remain relatively stable throughout a subject's lifetime, or at least stabilize once the subject reached maturity. Again, we can only wait for the full paper to be released to get the good doctor’s thinking about these findings.
The correlation between severity and the location of lesions with disease presentation is also fascinating. It will be quite enlightening to find out just which locations correlate with higher degrees of disability.
Perhaps the most tantalizing piece of info in the research summary is the declaration that CCSVI venous abnormalities are "not likely to directly trigger multiple sclerosis, but there may be another factor initiating the disease". One can only wonder at the evidence found that prompts this statement, which would suggest that CCSVI treatment alone may not put the much hoped for kabosh on the MS disease process. Then again, perhaps taking venous abnormalities out of the picture will halt the disease despite whatever other factors may be present.
I guess we'll just have to stay tuned for the release of the full paper for all of these questions to be answered. In all likelihood, though, as with practically all research related to MS and to CCSVI, the full paper will raise at least as many questions as it answers. Grrrrr...