A review by Kristen Cuenca, RNC, MSN, Case Manager WorldMed Assist of editorial “Multiple Sclerosis and CCSVI: The Neuroimaging Perspective” by M. Filippi, M.A. Rocca, F. Barkhof, R. Bakshi, F. Fazekas, O. Khan, D. Pelletier, A. Rovira, J. Simon in American Journal of Neuroradiology, published 2/3/11.

The editorial was intended to be a commentary on the contributions provided thus far “by MR imaging and other neuroimaging studies in shedding light on the value of the CCSVI theory in MS.” After reading this editorial, I have to take issue with the authors’ conclusions. The editorial was a back and forth written argument between research articles published to date—for and against the CCSVI and MS theory. Those supportive of CCSVI findings and those less demonstrative, such as comparing Zamboni’s initial study (n=109) to the Buffalo study (n=500). Similarly, the authors continued into the next section in the editorial addressing neuroimaging studies directly assessing the CCSVI theory. The first study attempted to refute CCSVI theory, although utilizing sophisticated MR angiography with 3 Tesla technology. The study only had 21 MS participants and 20 control participants. Generalizability of these results would be scientifically inaccurate.

Reference is then made to the studies evaluating iron deposition in the gray matter of the brain. Studies looking at aging brains and brains of MS patients were compared, demonstrating that older participants had iron deposition as well regardless of MS diagnosis. The authors also discussed studies which identify the relationship between plaque location and central nervous system vasculature in MS. The authors conclude that venous occlusion as with CCSVI, should result in brain swelling and hemorrhagic or ischemic infarctions—but these are not seen in the demyelinating plaques of MS patients. The authors described findings which point toward the presence of inflammation –related vasodilation of vessels, especially during the acute stage of brain lesion formation.

In addition, research was quoted to support the notion that the disease process of MS itself causes venous narrowing and stenosis. These venous changes were explained to have arisen from an adaptive physiologic response to low intracranial vascular (arterial) flow and low brain metabolism.

Regarding these hypothesized mechanisms for the resultant venous issues in MS—the question remains “which came first, the chicken or the egg?”. Although these scientific questions are worth pursuing, it does not negate the significant changes in symptoms of MS patients after said veins are treated with venoplasty. Check out www.ccsvi-tracking.com ---there are more than 600 patients who have logged symptoms in and many have found some improvement after endovascular treatment and THEY are significant! Perhaps the location of the brain in the body itself precludes the venous congestion they have hypothesized should occur—have we considered the effect of gravity? Do we fully understand how the blood brain barrier works?

Referring to a previous article I have reviewed (http://ccsvi-ms.ning.com/profiles/blogs/the-impact-of-simple-truncular), these venous abnormalities are congenital in origin. Are they exacerbated by the disease process of MS? Most assuredly….

Furthermore, what about those people who have CCSVI and have no symptoms or do not have MS? This is certainly not an unusual finding in the field of medicine. What about people with a positive ANA but no rheumatologic disease? They have no symptoms. What about people with Rheumatoid Arthritis and have NEGATIVE bloodwork for rheumatoid factor (RF)? They have symptoms, but no antibodies to demonstrate illness.

In my opinion, it will be difficult to end with a black and white response to the relationship of CCSVI to MS. But as with many diseases, patients are treated based on CLINICAL symptoms. Just something to think about as the back and forth conversation continues….

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